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From: TSS ()
Date: March 31, 2007 at 1:27 pm PST

'In the hands of God'
Thursday, March 29, 2007
Dr. Gregory J. Bever, 54, died Tuesday morning, at his home on Linwood Beach, surrounded by his family. His death was the result of a rare neurological malady called Creutzfeldt-Jakob disease. It struck suddenly and progressed rapidly.

Greg's sense of humor and selfless attitude persevered until the end, loved ones say.

Those who knew Greg best say he lived his life according to his heart's desires, mastering the endeavors he enjoyed most. He was a family man, a master dentist, a guitar player, a hockey booster and a sharp-shooter.

''He never denied himself anything,'' his wife, Lynne, says. ''He balanced his band, his work, the gun club. He loved his practice, his patients, and he did what he loved.''

Says brother Michaell Bever, of Atlanta, Ga.: ''He was focused on his family, his kids and his wife.''

He made time for others, leading groups of kids on Jet-Ski outings, or taking in relatives who needed temporary shelter. ''I never have known any human being that is so generous,'' Michaell says.

Molly Ballor, who's been office manager for Bever's practice for 22 years, says the staff at the bustling practice was part of his family, too.

''We feel like we've been kicked in the stomach,'' she said Tuesday. ''But we're doing what he'd want us to do: We're taking care of our patients.''


When Greg returned from the Mayo Clinic less than a month ago, word spread about the gravity of his condition, and well-wishers came calling at a rate of 30 to 40 a day.

Page 2 of 10
Pharmacist Tom Zsenyuk, Greg's best friend since they were freshmen at the University of Detroit, came from California.

''He was a special guy, very happy-go-lucky guy, and everybody liked him,'' Zsenyuk says. ''We used to play jokes on each other, and it was even better if there was a third party befooled.''

The two friends didn't speak of the illness during their final visit.

''It was just amazing to see him surrounded by so much love, from his family, his extended family,'' Zsenyuk says. ''I gave him a guitar pick that said 'We'll be friends forever.'''

The outpouring from friends and neighbors did not let up.

Greg was touched by the displays of friendship, but retained his levity.

''He turned to me and said, 'Lynne, this funeral is taking too long,''' says his wife of 26 years.

It's that sense of humor that's helped Greg and his family - which includes Gregory Jr., 19, a sophomore at Albion College; and All Saints students Alyson, 16, and Ian, 14 - face the grim diagnosis with grace.

''They're strong,'' Lynne says. ''They'll get through this.''


Page 3 of 10
Creutzfeldt-Jakob disease, according to the Centers of Disease Control and Prevention, strikes one person in a million worldwide.

The diagnosed disease was ''sporadic,'' which means it was not caused by anything that researchers have been able to pinpoint. It is not contagious. Most patients live less than a year after diagnosis, experts say.

For some unknown reason, proteins in CJD patients' brains fold in upon themselves, becoming something doctors call ''prions,'' and eat away at the healthy brain tissue.

Saturday, discussing her husband's illness with a Times reporter, Lynne held a brain-scan transparency up on a living room window overlooking the Saginaw Bay.

''You can see it so clearly when you know what you're looking for,'' she says, indicating porous-looking edges and an almost triangle-shaped white spot on the brain's right lobe. ''It turns brain tissue into sponge.''


Looking back, Lynne says, Greg's first symptoms probably appeared during a 10-day sailing trip to the British Virgin Islands in January. The first three days of the trip marked the first time the couple vacationed apart from their children since the first one came along 20 years ago.

Then the entire crew of family and friends arrived, and the group chartered three sailboats for a weeklong Caribbean island-hopping adventure. The sailing was rough, the weather hot, and the sleeping quarters were cramped.

''Greg's job was to man one side of the ropes, something he's done many times before,'' Lynne says. ''But he really couldn't do it. He'd loosen when he was supposed to tighten, or tighten when he was supposed to release. I thought, 'Wow, this lack of sleep is really affecting him.' He just kind of laughed it off.''

After returning to Linwood, Greg canceled his dental appointments and tried to get some rest.

Page 4 of 10
But his confusion persisted, so Greg drove himself to the emergency room at Beaumont Hospital in Troy.

Doctors there said Greg had suffered a stroke.

But his symptoms grew worse. He was sleeping 20 hours a day. He began having odd twitches and spasms, first with a thumb, then the whole hand. His arm torqued wildly one day when he and Lynne were sitting on the couch.

''What just happened?'' he asked her.

By early February, Greg's weight loss had reached 30 pounds. But a doctor assured the Bevers that within weeks, maybe months, he'd be back to normal.

After a Valentine's Day return to Beaumont, where more tests and a change of medication were ordered, Lynne says she became a bit pushy. She wanted an answer. She wanted her husband well.

The doctors said they had nothing more to offer.


One day toward the end of February, Lynne took Greg to the emergency room in Midland. A neurologist told Lynne that the lesion on the left side of Greg's brain was not from a stroke.

''It could be Creutzfeldt-Jakob disease,'' the neurologist said.

Page 5 of 10
A referral was made to Mayo Clinic, in Rochester, Minn.

Lynne packed her bags with two weeks of clothes. Surely, she thought, it's something else. Maybe Parkinson's, something curable. Or at least treatable.

''They were going to find out what was wrong with him, and he'd get some intensive rehab,'' she says, recalling her mindset as she made plans to go to Minnesota.

When they arrived in Rochester, they were met by a man who'd been arranged by Lynne's employer, AstraZeneca Pharmaceuticals, to rush them to the hospital. Greg's stiffness and uncontrolled movements had grown worse.

''Doctors and nurses were all over him, like something from a movie,'' Lynne says.

Doctors tried three different medications, to no avail. Greg spun and thrashed in the bed, asking ''What's happening to me?''

A day later, a brain scan led doctors at Mayo to diagnose CJD, Lynne says. It's fatal, doctors told them. There is no treatment, no cure.

''I guess it sucks to be me,'' Greg responded, mostly to break the tension in the room.

Doctors were concerned about Greg's rapid deterioration.

''How close are your kids?'' one asked.

Page 6 of 10

A few phone calls later, the Bever children, along with Lynne's brother, John Zessin were on a small plane, piloted by one of Greg's dental patients and family friend Mark VanBenschoten. Through snow squalls, they sped across Lake Michigan toward their father.

The teens already knew their dad was sick.

''What you don't know is that there's no cure for this disease,'' the doctor said. ''He's going to die.''

The tears came, and then the hugs. And these words from Lynne, words that the family has lived by since.

''This disease is so rare,'' she said, ''let's look at it as a gift.''

''We have time to say good-bye. Just think, if he was killed in a car accident on the way home from work one day, we wouldn't have been given this time.''

And so the good-byes began, the teens taking turns having time alone with their dad in the hospital room.

''Fourteen years was not enough time to have together,'' Ian told his dad.

''Buddy,'' Greg said, ''if I had 40 more years to spend with you, that still wouldn't be enough.''

Page 7 of 10
Greg wanted to go home.

The return trip was arduous. Greg was so stiff, Lynne says - ''basically, 180 pounds of immovable man'' - he had to be loaded into his seat through the cargo door.

Before leaving Rochester, Lynne called a friend who's a state trooper, asking if he could line up a stretcher. When they arrived at the airport, an ambulance and three attendants were waiting to take Greg home.

When he saw the hospital bed they had waiting for him, he wanted no part of it.

''I'm not using that,'' he said.

He never did.


The dentist started a rock band at the age of 44, when he and three friends formed the classic-oldies group The Sinclairs.

''It was his vision and passion for oldies music that led us to start the band,'' says guitar player Rod Loomis, of Midland. ''His vast library of nostalgia, facts, dates, and details for '60s music... The man was a walking library. He was amazing.''

The band, including drummer Ken Gloss and singer Dennis Beson, worked up a set of such standards as ''Secret Agent Man'' and ''I Fought the Law.'' They grew popular, playing up to 15 weekends a year.

Page 8 of 10
''Greg had boundless energy,'' Loomis says.

Greg's ''guitar room'' is where he'd practice, with a half-dozen classic instruments housed among an array of memorabilia of the Beatles, his favorite band.

The last time Greg picked up a six-string - as the illness was taking hold - he came back downstairs, disgusted.

''He said he couldn't find the chords,'' Lynne says.

Shooting was another of Bever's passions. A member of the Linwood-Bay Sportsman's Club, Greg earned titles in skeet-shooting and shared his passion by teaching newcomers the sport.

An annual pheasant-hunting trip to South Dakota with brother Bruce each October was a 34-year tradition and a bright spot on Greg's calendar.

''We were hunting and motorcycle buddies,'' says Bruce, of Marietta, Ga. ''We made an awesome team.''

When someone suggests that Greg was a perfectionist, Michaell sets the record straight.

''No, that's not right,'' Michaell says. ''He's a person who believed in excellence. He didn't expect perfection from himself or from anyone. He's a man who knew the difference between perfection and excellence.''

''But,'' adds Lynne, ''he was a master at everything he did.''

Page 9 of 10
In 1999, Greg became the 19th dentist in Michigan to obtain the prestigious designation as ''master dentist'' from the Academy of General Dentistry, the culmination of 10 years - 1,100 hours - of study beyond his dentistry doctorate.

Greg told a Times reporter in 1999 where his work-ethic came from.

''My mother always said if you're going to be a ditch digger, be the best ditch digger,'' Greg said.

''It's just a commitment to excellence. I think excellence is an attitude that pervades all through your life.''


Lynne met Greg, a Plymouth native, at her father's dairy near Detroit when she was just 17. Greg, six years her senior, was completing a biology degree. They were married in 1980, and Greg graduated from dental school at Marquette University in Milwaukee, Wis., in 1984.

Greg went into partnership with dentist Jack Dee in Freeland and a year later, opened his own practice in Linwood.

''From the very first day,'' Lynne says, ''he was booked three weeks out.''

The Bevers fell in love with Linwood, and bought a little place on the beach. They've since built a new house - a sunny brick-faced home with windows looking out on the bay.

Greg bought out a small practice in Bay City, then, 15 years ago, merged the two offices into the current location, at 3926 Traxler Court, in Monitor Township.

Page 10 of 10
Lisa Moss, a dentist from Novi, has been seeing patients there since February and will continue to treat his patients until another dentist purchases the practice, Ballor says.


Greg's family will receive visitors from 2 p.m. until 8:30 p.m. today at the W.A. Trahan Funeral Chapel, 256 N. Madison. A prayer vigil is planned for 7 p.m. On Friday, the Rev. Robert DeLand will lead the funeral Mass at 10 a.m. at St. James Church, 710 Columbus Ave.

Lynne recalls a bit of advice one of her friends offered shortly after Greg's diagnosis.

''I hope you're not trying to find an answer,'' the friend said. ''Because there is no answer to find.''

Lynne decided to waste no time with the torture of ''Why?''

''It was in the cards a long time ago,'' she says. ''We've put it in the hands of God.''

- Crystal Harmon can be reached at 894-9643 or by e-mail at

Subject: SEAC Position statement vCJD and Endodontic dentistry
Date: May 8, 2006 at 6:45 am PST
TSS 2005
SEAC Position statement vCJD and Endodontic dentistry
Mon May 8, 2006 09:08

Position Statement


Position statement vCJD and Endodontic dentistry

1. The Department of Health (DH) asked SEAC to advise on the findings and implications of a preliminary risk assessment of potential vCJD transmission via endodontic procedures (dental procedures involved in the maintenance of dental pulp and the treatment of the pulp cavity) 1. This is particularly pertinent because of the large number of endodontic procedures undertaken in the UK.


2. There are no reported definite or suspected cases of vCJD transmission arising from dental procedures. However, prions are more resistant than other types of infectious agent to the conventional cleaning and sterilisation practices used to decontaminate dental instruments 2. Therefore, should dental instruments become contaminated from tissues in the oral cavity of infected individuals, there is a risk of transmission to subsequent patients.

3. A quantitative DH risk assessment 3, accepted by SEAC in 2003, considered two possible mechanisms for the transfer of vCJD infectivity via dental instruments: (i) accidental abrasion of the lingual tonsil, known to carry infectivity in vCJD cases; and (ii) contact with dental pulp that evidence from animal studies suggested may be infective. On the basis of the information available, the DH analysis suggested that the risk of transmission to individual patients via accidental abrasion of the lingual tonsil is very low. Furthermore, should dental pulp be infective, the risk of transmission via endodontic procedures, although higher, is also low. Although a very large number of dental procedures are conducted, the relative risk to public health from potential transmission via dental, compared with hospital, surgery was considered to be relatively low.

4. In 2006, SEAC considered a new preliminary risk assessment by DH of the risks of vCJD transmission via endodontic procedures, taking into account new information on decontamination of dental instruments, the potential infectivity of dental pulp, and the possible existence of subclinical vCJD carrier cases.

Endodontic instruments

5. Evidence suggests that the files and reamers used in endodontic procedures are reused and are difficult to reliably decontaminate 4. Appreciable quantities of residual material remain adherent to the surface after normal cleaning and sterilisation 5. Thus, there is potential for transfer of dental pulp between patients undergoing endodontic procedures.

vCJD infectivity in dental tissues

6. There are no data on vCJD infectivity in dental pulp. Although no abnormal prions were found in a study of dental tissues, including dental pulp, from vCJD cases 6, dental pulp includes blood and peripheral nerve tissue known to carry vCJD infectivity 7,8. In addition, appreciable infectivity has been found in the dental pulp of hamsters with hamster scrapie 9. Although it is possible that the peripheral nerve may only become infective close to, or after, the onset of clinical vCJD, inflammation may promote the propagation of prions 10. Thus, although the data are limited and indirect, it is reasonable to assume that the dental pulp of individuals subclinically-infected with vCJD may be infectious although the level of infectivity is unknown. Studies underway will provide direct data on the infectivity in dental tissues from vCJD cases.

Subclinical carrier state

7. A study of humanised mice showed that vCJD infections may not always progress to clinical disease within the normal lifespan of the animals 11. Another study suggested that prion infections in mice that remain at a subclinical level can be transmitted to other mice, resulting in clinical disease 12. Thus, there is evidence to suggest that individuals infected with the BSE / vCJD agent may remain in a subclinical infection carrier state instead of developing vCJD. A discrepancy between prevalence estimates based on a survey of abnormal prion protein in appendix and tonsil tissue and data on vCJD cases supports this hypothesis 13. As no diagnostic test exists to identify such individuals, they could over the course of their lives be potential sources of numerous secondary infections arising from invasive medical or dental procedures.

8. The prevalence of subclinical infection in the UK population is uncertain. A recent estimate suggests the number of subclinical carriers may be of the order of several thousand 14. SEAC has strongly recommended that further studies to ascertain better the prevalence of vCJD infection be urgently considered 15.

Transmission risks

9. The new DH analysis suggests that, on the basis that residual dental pulp on endodontic files and reamers is transferred relatively efficiently to patients on reuse, dental pulp is as infective as peripheral nerve tissue and a subclinical carrier population for vCJD exists, a self-sustaining vCJD epidemic arising from endodontic surgery is plausible. There are uncertainties about the efficiency of vCJD transmission via endodontic procedures, the vCJD infectivity of dental pulp and the existence of a subclinical infection carrier state. However, even if a self-sustaining epidemic were not possible, clusters of vCJD infections could arise from the use of instruments contaminated with the vCJD agent from endodontic procedures on infected patients. Interactions between this and other routes of secondary transmission, such as blood transfusion and hospital surgery, would make a self-sustaining epidemic more likely.

Potential risk reduction measures

10. Endodontic files and reamers have a limited lifespan, restricting the number of possible secondary transmissions. Improving the effectiveness of procedures used to decontaminate dental instruments would reduce the risk of transmission. Restricting endodontic files and reamers to single use would prevent potential secondary transmission via these instruments.


11. A preliminary risk assessment produced by DH suggests that vCJD transmission via endodontic dentistry may, under certain hypothetical but plausible scenarios, be sufficient to sustain a secondary vCJD epidemic. However, there are uncertainties around the data and assumptions underpinning the assessment. Research underway will address some of these uncertainties and allow the risk assessment to be refined. Once the research is complete and / or other data become available, the risks should be reassessed. A watching brief should be maintained.

12. It is unclear whether or not vCJD infectivity can be transmitted via endodontic files and reamers. However, given the plausibility of such a scenario and the large number of procedures undertaken annually, it would be prudent to consider restricting these instruments to single use as a precautionary measure. Since sufficiently rigorous decontamination of these instruments is difficult, single use of these instruments would eliminate this risk, should it exist.

May 2006


1. Department of Health. Dentistry and vCJD: the implications of a “carrier state” for a self-sustaining epidemic due to endodontic dentistry. A Preliminary Risk Assessment. Unpublished.
2. Smith et al. (2003) Prions and the oral cavity. J. Dent. Res. 82, 769-775.
3. Department of Health. (2003) Risk assessment for vCJD and dentistry.
4. Letters et al. (2005) A study of visual and blood contamination on reprocessed endodontic files from general dental practice. Br. Dent. J. 199, 522-525.
5. Smith et al. (2005) Residual protein levels on reprocessed dental instruments. J. Hosp. Infect. 61, 237-241.
6. Head et al. (2003) Investigation of PrPres in dental tissues in variant CJD. Br. Dent. J. 195, 339-343.
7. SEAC 91 minutes paragraph 9.
8. Department of Health (2005) Assessing the risk of vCJD transmission via surgery: an interim view. Unpublished.
9. Ingrosso et al. (1999) Transmission of the 263K scrapie strain by the dental route. J. Gen. Virol. 80, 3043-3047.
10. Heikenwalder et al. (2005) Chronic lymphocytic inflammation specifies the organ tropism of prions. Science. 307, 1107-1110.
11. Bishop et al. (2006) Predicting susceptibility and incubation time of human-to-human transmission of vCJD. Lancet Neurology.
12. Hill et al. (2000) Species-barrier-independent prion replication in apparently resistant species. Proc. Natl. Acad. Sci. USA. 97, 10248-10253.
13. SEAC Epidemiology Subgroup (2005) Position statement on the vCJD epidemic.
14. Clarke & Ghani. (2005) Projections of future course of the primary vCJD epidemic in the UK: inclusion of subclinical infection and the possibility of wider genetic susceptibility. R. J. Soc. Interface.
15. SEAC (2005) SEAC response to the SEAC Epidemiology Subgroup statement on the vCJD epidemic.

Page updated: 8th May 2006

Dental treatment and risk of variant CJD – a case control study

D. Everington,1 A. J. Smith,2 H. J. T. Ward,3 S. Letters,4 R. G. Will5 and J. Bagg6

Objective Knowledge of risk factors for variant CJD (vCJD) remains

limited, but transmission of prion proteins via re-useable medical devices,

including dental instruments, or enhanced susceptibility following trauma

to the oral cavity is a concern. This study aimed to identify whether

previous dental treatment is a risk factor for development of vCJD.

Design Case control study.

Methods Risk factor questionnaires completed by interview with

relatives of 130 vCJD patients and with relatives of 66 community and

53 hospital controls were examined by a dental surgeon. Responses

regarding dental treatments were analysed.

Results We did not find a statistically signifi cant excess of risk of vCJD

associated with dental treatments with the exception of extractions in

an unmatched analysis of vCJD cases with community controls

(p = 0.02). However, this result may be explained by multiple testing.

Conclusions This is the first published study to date to examine

potential links between vCJD and dental treatment. There was no

convincing evidence found of an increased risk of variant CJD

associated with reported dental treatment. However, the power of the

study is restricted by the number of vCJD cases to date and does not

preclude the possibility that some cases have resulted from secondary

transmission via dental procedures. Due to the limitations of the data

available, more detailed analyses of dental records are required to fully

exclude the possibility of transmission via dental treatment.



Many studies have searched for risk factors for the development

of different types of CJD, such as diet, exposure to

animals, surgical treatment, including dentistry, and occupational

exposures. A retrospective case control study15 of 60

definite cases of sporadic CJD, occurring in Japan between

1975 and 1977 found no association with extractions of maxillary

or mandibular teeth. An analysis of 26 sporadic CJD

cases and 40 matched controls from the United States16 failed

to discover a significant odds ratio for endodontic surgery,

though these workers did note statistically significant odds

ratios for intraocular pressure testing, injury to or surgery on

the head, face or neck and trauma to other parts of the body.

However, these findings suffer from low statistical power and,

in the case of the Japanese paper, information was requested

for extractions only during the fi ve year period prior to onset.

This paper attempts to identify an association between vCJD

and reported dental treatment.

Comparison of the reported dental histories of cases and

controls found that extractions were the only dental risk factor

that reached statistical significance (at the 5% level) in the

unmatched analysis with community controls. This may be a

result of multiple testing especially as there are fewer extractions

in the cases than in the hospital controls. It is likely that

the majority of vCJD cases in this cohort were infected through

eating BSE contaminated meat products. Therefore, it is diffi -

cult to detect a small subgroup that may have been infected by

secondary transmission, as in this study, through dentistry.

There are a number of limitations to this study, most importantly

relying on reported data from relatives and the relatively

small numbers of cases and controls resulting in low

power to detect statistical differences. Recruitment of controls

has been problematic,17 although every effort was made to

maximise this group. Selection of controls was not matched for

demographic and socio-economic factors for dental attendance

and this may have resulted in bias. It is possible that some of

the responses of ‘no known treatment’ reflect poor knowledge

or recall on the part of the relatives. This would reduce the

power of the study to pick up significant differences between

groups, but not necessarily introduce bias.

Whilst these preliminary data on a topic of great concern

for public health do not provide evidence supporting reported

dental work as being a major route of transmission of the BSE

agent to humans to date, they do not preclude the possibility

that some vCJD cases have been infected by this route.

Furthermore, the incubation period following infection by

a peripheral route may be relatively long and therefore the

period of observation to date of potential secondary transmission

of vCJD may be too short to detect cases.

A more detailed study of previous treatment based on reviewing

actual dental records rather than relying on reported treatments

is required to gain a wider insight into the dental history

of both cases and controls. We are currently investigating the

possibility of examining dental records of vCJD cases and a

larger group of unmatched controls.18

The National CJD Surveillance Unit is funded by the Department of Health

and the Scottish Executive Department of Health. The sponsors of the study

had no role in study design, data collection, data analysis, data interpretation,

or in the writing of the report. We are also grateful to the families of

cases, without whose co-operation this study would not have been possible.


Subject: PrPSc in salivary glands of scrapie-affected sheep
Date: February 15, 2007 at 9:33 am PST

J. Virol. doi:10.1128/JVI.02148-06
Copyright (c) 2007, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

PrPSc in salivary glands of scrapie-affected sheep

Marta Vascellari*, Romolo Nonno, Franco Mutinelli, Michela Bigolaro, Michele Angelo Di Bari, Erica Melchiotti, Stefano Marcon, Claudia D'Agostino, Gabriele Vaccari, Michela Conte, Luigi De Grossi, Francesca Rosone, Francesco Giordani, and Umberto Agrimi
Istituto Zooprofilattico Sperimentale delle Venezie, Histopathology Department, Viale dell'Università 10, 35020 Legnaro (PD), Italy; Istituto Superiore di Sanità, Department of Food Safety and Animal Health, Viale Regina Elena 299, 00161 Roma, Italy; Istituto Zooprofilattico Sperimentale delle Regioni Lazio e Toscana, Strada Terme, 01100 Viterbo, Italy

* To whom correspondence should be addressed. Email: .


The salivary glands of scrapie-affected sheep and healthy controls were investigated for the presence of the pathological prion protein (PrPSc). PrPSc was detected in major (parotid and mandibular) and minor (buccal, labial and palatine) salivary glands of naturally and experimentally infected sheep. By western blot, PrPSc concentration in glands was estimated as 0.02-0.005% of brain. Immunohistochemistry revealed intracellular deposition of PrPSc in ductal and acinar epithelium and occasional labeling into the lumen of salivary ducts. The presence of PrPSc in salivary glands highlights the possible role of saliva in the horizontal transmission of scrapie.

Subject: CJD: update for dental staff
Date: November 12, 2006 at 3:25 pm PST

1: Dent Update. 2006 Oct;33(8):454-6, 458-60.

CJD: update for dental staff.

Scully C,
Smith AJ,
Bagg J.
Eastman Dental Institute, University of London.

It is almost a decade since the recognition of the emergence of a new infectious disease termed variant Creutzfeldt-Jakob disease (vCJD) caused by prions (PrPTSE), abnormal variants of a normal human cell surface protein (PrP).This disease has a number of similarities to other forms of CJD--lethal disorders characterized by a prolonged incubation period, and progressive mental deterioration. In relation to oral tissues, PrPTSE have been found in neural, gingival, pulpal, lingual, lymphoreticular and salivary gland tissue in animal models. In both sporadic and variant CJD, PrPTSE is detectable in the trigeminal ganglion and, in vCJD, in lymphoreticular tissues, but infectivity has not been tested in other human oral tissues. CLINICAL RELEVANCE: PrPTSE is much more resistant to the common methods of inactivation than conventional pathogens, and it adheres avidly to steel whilst retaining its infectivity. Particular attention must be paid to cleaning and sterilizing re-usable dental instruments. Single-use devices, such as endodontic files and matrix bands, must never be re-used. Advice on the reprocessing of dental instruments used on known CJD patients must be obtained from local infection control teams. Research into effective methods of prion inactivation appears promising, although further work on the applicability to general dental practice is required.

PMID: 17087448 [PubMed - in process]

18 January 2007 - Draft minutes of the SEAC 95 meeting (426 KB) held on 7
December 2006 are now available.


64. A member noted that at the recent Neuroprion meeting, a study was
presented showing that in transgenic mice BSE passaged in sheep may be more
virulent and infectious to a wider range of species than bovine derived BSE.

Other work presented suggested that BSE and bovine amyloidotic spongiform
encephalopathy (BASE) MAY BE RELATED. A mutation had been identified in the


3:30 Transmission of the Italian Atypical BSE (BASE) in Humanized Mouse

Models Qingzhong Kong, Ph.D., Assistant Professor, Pathology, Case Western Reserve

Bovine Amyloid Spongiform Encephalopathy (BASE) is an atypical BSE strain
discovered recently in Italy, and similar or different atypical BSE cases
were also reported in other countries. The infectivity and phenotypes of
these atypical BSE strains in humans are unknown. In collaboration with
Pierluigi Gambetti, as well as Maria Caramelli and her co-workers, we have
inoculated transgenic mice expressing human prion protein with brain
homogenates from BASE or BSE infected cattle. Our data shows that about half
of the BASE-inoculated mice became infected with an average incubation time
of about 19 months; in contrast, none of the BSE-inoculated mice appear to
be infected after more than 2 years.

***These results indicate that BASE is transmissible to humans and suggest that BASE is more virulent than
classical BSE in humans.***

6:30 Close of Day One

1997 TO 2006. SPORADIC CJD CASES TRIPLED, with phenotype
of 'UNKNOWN' strain growing. ...

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

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



30. I cannot recall now when I first became aware of the new bovine disease but on

the 16th November 1988 I attended the CDSM to present two papers on dental products

[YB88/11.16/6.1-6.7]. At that meeting and the Committee noted a paper which provided

a background to the problem of BSE (YB88/5.13/9.1).


31. On the 15th March 1989 [YB89/3.15/7.1-7.3], I attended the CDSM because there

were two items (items 11 and 23) on the agenda of dental interest which I had prepared

papers for.

32. At this meeting the Joint CSM/VPC Guidelines [YB89/3.00/1.2] for Industry

paper relating to BSE was noted and the Southwood Report IBD 2[vol IBD1, tab 2] was

given to members to take away [YB89/3.15/7.2].

33. On the 16th March 1989, I wrote to Dr Adams (Principal Medical Officer,

Medicines Division with overall responsibility for the review of medicines and the

CDSM) [YB89/03.16/8.1]. I had read the Joint CSM/VPC Guidelines [YB89/3.00/1.2]

and asked for an explanation of the sterilization guidelines which were in excess of the

Department of Health guidelines for sterilisation of unwrapped instruments. The length of

time in the Joint Guideline for autoclaving using a porous load cycle at 134-138 degrees

was 18 minutes instead of the usual minimum of 3 minutes.

34. I suggested to Dr Adams in that minute that in view of the comments that were

made with regard to the undesirability of harvesting human dura, this had implications for

the sterilization of all instruments used routinely for cranial surgery. Because the Joint

CSM/VPC Guidelines for Industry were to be sent to overseas manufacturers, I

questioned whether the units for pressure should have been expressed in the international

SI (Standard International) units.

35. Dr Adams in his minute dated the 21st March 1989 [YB89/03.21/15.1], stated that

the sterilization details were provided by MAFF at the Central Veterinary Laboratory and

seen by the Expert Working Group on BSE. He stated that advice along similar lines had

been issued to the NHS in 1981. There had been a number of well documented cases

where CJD had been transmitted via the use of contaminated instruments. He stated that

he was sure that these cases would be known to neurosurgeons.

36. I was minuted by Dr Pickles on the 17th April 1989 [YB89/4.1/5.1]. She

mentioned some comments made by the Tyrrell committee when considering the CSM

Guidelines and Dr Will’s concern in relation to topical dental products. I cannot recall

whether I wrote in response to this minute. I believe that I took it to be a notification of

the need for vigilance should dental products that had bovine actives/intermediates

become available and application made for licenses.


37. I attended the CDSM meeting on the 17th January 1990 [YB90/1.17/12.1-12.5]

because applications for licences for dental products were being considered by the

Committee. It was usual for assessors to be asked to report on anything of a general

nature at the end of the discussions on papers. On this occasion the Committee were

informed that an application had been received under the Committee for Proprietary

Medicinal Products arrangements and the UK would be taking the lead. This was an

arrangement whereby a simultaneous application for a product licence could be made by

a company to a number of European Countries. The Committee was advised that it would

have to consider this application later in the year.


38. At the Meeting of the CDSM held on 20th November 1991 [YB91/11.20//6.1-6.4] I

presented my assessment of a product consisting of a mixture of bovine derived collagen

and hydroxyapatite for the augmentation of deficient alveolar ridges. CDSM were unable

to advise the grant of a product licence.


39. I attended the meeting of the CDSM held on 21st July 1993 [YB93/07.21/4.1-4.7]

to present the assessment of a collagen based product. The Committee were unable to

advise the grant of product licence.

40. On 13th September 1993, Mr Eaton, another Senior Dental Officer (with

responsibility for hospital dental services and postgraduate and continuing dental

education) minuted me [YB93/9.13/2.1] in relation to a request he had received from Dr

Ailsa Wight which required comment on an CJD article in the Daily Express dated 4th

September [YB93/09.04/3.1]. Mr Eaton had contacted a Professsor of Dentistry who

stated that it was most unlikely that treatment procedures in General Practice could be

responsible for transmission of CJD. He asked me to comment on a brief paper about

CJD which had been prepared by Dr Wight.

41. On the 14th September 1993 I minuted Dr Ailsa Wight (Senior DH medical officer

and SEAC Observer) [YB93/09.14/5.1]. I wrote that it seemed extremely unlikely that a

dentist in General Practice could infect patients with CJD virus. This statement was based

on the fact that human dura was not used in general dentistry but had been used in

specialised oral surgery which would not be carried out by a dentist in general practice.

42. I also informed Dr Wight that collagen sponge of bovine origin was commonly

used at one time as a haemostat following dental extractions. I stated that as far as I was

aware, no such dental products were licensed in the UK at that time.

43. I was able to give the advice in this minute from knowledge of what constituted

the general practice of dentistry, knowledge of dental products which I had gained from

my work as a general practitioner and as a senior dental officer which involved keeping

"up-to-date" with dental practice.

44. On the 28th September, Mr. Gordon had written to Dr Wight in relation to a

proposed BDA publication [YB93/09.28/3.1-3.3]. Dr Wight sent me her draft reply to Mr

Gordon and I made two minor comments in a minute dated 1st November 1993

[YB93/11.01/5.1]. I recommended that her reply should include a suggestion that the

BDA paper on Iatrogenic Creutzfeldt-Jakob Disease, should include there were other

good reasons for considering many endodontic instruments as single use items and for

limiting the number of times others might be re-used.

45. I remember that these reasons included the fact that re-sterilization of these

instruments might affect the physical properties of the instrument. The re-sterilization

might increase the chances of fracture of such instruments in the root canal. This would

have given rise to considerable difficulty in achieving a satisfactory result as far as a

patient was concerned. There were other amendments and according to letters I was

copied, the BDA publication was amended by Mr Gordon [YB93/11.17/5.1-5.4].


46. I left the Department of Health in May 1994.

Relevant interests

47. I have no links past or present with the farming community, renderers, feed stock

manufacturers, pet food manufacturers, trade associations. During my time at the

Department of Health I had contact with pharmaceutical companies in a solely

professional capacity. Since leaving the DH, I have done part time consultancy work for a

number of manufacturers who produce dental products though none have been involved

with products of bovine origin.

48. This Statement is true to the best of my knowledge and belief.

Issued on behalf of the witness by:

The BSE Inquiry Press Office

6th Floor Hercules House

Hercules Road

London SE1 7DU

Fax: 0171 803 0893


Possible occupational risks from TSEs

Although CJD has been documented in a neurosurgeon, two neuropathology technicians, an

orthopaedic surgeon and a pathologist, it is reassuring to note that in none of these individuals

was there a history of a definite infective event. The orthopaedic surgeon had however worked

with human and ovine dura mater 20 years prior to his illness. Case-control studies do not

suggest that individuals potentially exposed to the TSE agent in the health care setting are at an

increased risk of developing CJD. However, the possibility that cases of CJD have rarely

occurred in such circumstances cannot be confidently dismissed.

A statistically significant excess of cases of CJD in cattle farmers has been reported in the UK

since 1990. Of concern, four of these six cases were known to have had BSE-affected animals in

their herds. However, analysis of the clinical and pathological features of these cases showed that

none had the nvCJD phenotype. This observation has been strengthened by recent molecular

biological data that demonstrated that the PrP glycosylation pattern characteristic of both BSE

and nvCJD was not present in any of these cases. Furthermore analysis of the incidence of CJD

in dairy farmers from other European countries, in which BSE is rare or absent, reveals a similar

excess of cases. This observation suggests that dairy farmers may be at increased risk of CJD for

reasons other than exposure to the BSE agent. One possible explanation for the apparent excess

of cases in dairy farmers, particularly in the UK, is that case ascertainment in this group has been

better than in other groups because of concern of a possible link between the bovine and human




It is of great concern that there may be a risk of becoming infected with nv-CJD in the dental

surgery due to cross infection from either the dentist or another patient. The two main sources of

infectious material in the dental surgery are blood and saliva. As shown in Table 7 these are of

relatively low infectivity compared to the tissues of the CNS.

As nv-CJD has only recently been discovered, few experiments have been carried out to discover

whether it can be transmitted. Therefore, we must look at the other TSEs to get an indication of

likely risk.

The risk of transmission via saliva

Studies to ascertain levels of PrP have shown that salivary gland tissue contains high levels of

infectivity, much earlier than in brain tissue (Sakaguchi 1993, Eklund 1967). Replication of the

infectious agent first appears in salivary tissue soon after inoculation, possibly indicating that the

salivary glands are one of the primary sites of replication, rather than the brain. It was also found

that infectivity declines with time, suggesting that greatest risk from transmission is likely to be

early in the disease, before clinical signs are present.

There has been no research into the risk of transmission from saliva, however we must assume

that if salivary gland is infected then so is the saliva it produces.

The effect of gingival scarification on transmission

If it is found that BSE has been transmitted to humans via the oral route it is essential to ascertain

any factors that may have increased susceptibility and therefore may have implications for

human to human transmission. Studies into the effect of gingival scarification on the

transmission of Scrapie (Carp 1982) have shown that a higher proportion of mice succumbed to

infection if their gingivae had been scarified compared to the controls (100% and 71%

respectively). It was also shown that the incubation period was significantly shorter.

Although it has not been possible to transmit Scrapie using dental burs (Adams 1978) it was

found that the gingivae of infected mice do contain a low level of Scrapie infection that can be

transmitted using an intra-cerebral approach.

The risk of transmission via blood products

Although most forms of CJD have been considered infectious by the mid-1960s its

transmissibility through the use of blood products is still controversial.

Sporadic CJD has been reported to be transmitted to mice by injecting blood from human

patients directly into mouse brain (Brown, 1994, Manuelidis, 1985). However this evidence has

not been reproduced and another review of research with non-human primates indicated that

sporadic CJD-infected human blood did not transmit the disease to primates (Tateishi, 1985).

Some evidence indicates that blood of experimentally infected animals contains an infective

agent. PrP infectivity resides predominately or exclusively in lymphocytes and monocytes rather

than granulocytes (Lavelle, 1972). There has been no evidence of infectivity in erythrocytes,

platelets or plasma, but low infectivity cannot be excluded. Animal studies have demonstrated

that the scrapie-agent replicates first in the spleen and other lymphoid tissues but reaches the

highest concentration in the brain, where it results in the clinical appearance of the disease

(Kurudail 1983). Hence, peripheral tissues in contact with blood also harbour PrP infectivity.

Animal transmission data indicate that human spleen, lymph nodes, serum and cord blood are

irregularly infective for animals, although few cord blood samples have been tested (Manuelidis,

1979). Studies of experimental sporadic CJD in guinea pigs and mice have shown that the

infectious agent is present in the brain, viscera and blood before clinical disease develops

(Lavelle, 1972 & Czub 1986).

Several factors must be considered in reviewing the animal evidence regarding transmission of

human TSEs in blood: the type of human TSE being tested, the level of PrP infectivity of the

study tissue, the species barrier, and the route of transmission.

The evidence from animal studies is inconclusive regarding transmission of sporadic CJD

between humans by transfusion.

Although case reports have provided evidence linking CJD to the receipt of dura mater and

human growth hormone, no human cases have yet been causatively linked to blood transfusion.

A number of cases have been seen where patients have undergone organ transplant and then

developed CJD. It is, however, impossible to determine whether the organ was the source of the

infection as insufficient information about each case is available.

If CJD is transmissible in blood, cases should occur in young patients, particularly if the

incubation period is short as in the other iatrogenic cases. Even if the incubation period were

many years, one would expect to see cases in young persons because of the transfusions given to

infants and young children. If CJD is transmitted in blood, a detectable increase in cases in blood

transfusion patients may be expected. There is a ban on the use and export of blood and blood

products from the UK (February 1998) as a precautionary measure and for the past two years any

donor with a family history of CJD has been prevented from donating blood. However this may

be unreliable, as many patients will not know the accurate diagnoses of a family member's


As noted by Brown (1996) in reference to blood products, "iatrogenic disease from this source

would dwarf in importance all other sources by virtue of the sheer numbers of people who

theoretically have been or could be at risk". The appearance of nvCJD raises new concerns. Due

to a possible oral route of infection and a novel strain of agent, the distribution of tissue

infectivity may differ from other forms of CJD. This is supported by evidence that suggested that

at the palatine tonsil might harbour PrP in nvCJD but not in sporadic CJD.

In view of the theoretical possibility that blood from patients incubating a TSE may harbour the

infective TSE agent the World Health Organisation recommends that the following groups

should be excluded as blood donors:

· Recipients of extracts derived from human pituitary glands (growth hormone and


· Those with a family history of CJD, GSS or FFI.

· Those who have received a human dura mater graft.

Animal studies indicate that the infective agent of human TSEs is present in blood in low titres,

and sufficient evidence of animal transmission suggests that the disease has the potential to be

transmitted through blood (Heye 1994). However, to date, epidemiological evidence indicates

that if blood transmission occurs it is likely to be rare. This may be due to polymorphism at

codon 129, which could restrict susceptibility. It is also possible that most transfusions may not

contain sufficient dose to cause infection.

There is no specific scientific evidence to date that nv-CJD will transmit through blood products.

This is due to the incubation period being many months in laboratory animals. As infectivity has

only been detected in white blood cells the potential risk from donated blood can be decreased by

a process known as leuko-depletion, removal white blood cells.

The knowledge that blood may be infected could change the views of both the medical

profession and patients. Transfusions may only be used if absolutely necessary and patients may

be given the option of donating their own blood for scheduled operations.

If CJD were transmitted in pooled blood products or saliva, clusters would be detected. Most

clusters have usually been attributed to familial disease (Masters, 1979 & Reingold 1996).

Surveillance systems have found cases of CJD among persons who have received blood

transfusions but none have been linked to blood transmission.

It must be remembered, however, that surveillance systems may not detect cases when unique

epidemiological or clinical features are present.


A number of factors must be taken into consideration when assessing the risk of transmission of

nvCJD during dental treatment. Dental patients are at risk of infection from a number of sources,

the most significant being the consumption of infected animal products during the 1980s. A

small minority of patients will also be at increased risk in their place of work, such as

neuropathologists, neurosurgeons and laboratory technicians.

The most likely route of infection is via ineffectively sterilised instruments. If a patient is

suspected of having or has been diagnosed with nv-CJD further precautions can be taken. The

patient is likely to be showing clinical signs, which are likely to make dental treatment difficult,

therefore only emergency treatment is going to be appropriate. Where possible, a treatment

option that involves the least cross infection risk should be undertaken. . To reduce this risk, all

instruments that have been used on a patient with nvCJD should be disposable or discarded. This

includes oral surgery equipment, root planing hand instruments and ultrasonic tips in addition to

needles and blades. In the case of accidental inoculation it is unlikely that sufficient infective

material will be involved to transmit the disease. As discussed previously, the peripheral route of

infection is ineffective compared with intracerebral inoculation, and blood or saliva contains

little infectivity compared to central nervous tissue. All patients should be treated using universal

precautions, which should be employed in all dental practices as a matter of routine, providing

the maximum protection equally to clinical staff and patients. This includes the use of gloves,

masks and eye protection at all times. After each patient all instruments should be autoclaved and

disposable alternatives should be used where appropriate.

The number of patients likely to be incubating nv-CJD is impossible to predict at present. Much

depends on the average incubation time, the longer the time, the higher the figure is likely to be.

At present the average incubation time can not be calculated nor is it possible to estimate the

dose required to infect a human. With the possibility of a nationwide epidemic investigation

must be carried out to determine the risk from cross infection. Research has yet to prove that

there is a risk, however, until all possibility of this can be discounted caution must prevail.

The resistance of the TSE agent to standard medical sterilisation procedures is noteworthy.

Experimental evidence demonstrates that the agent shows resistance to the following: exposure

to boiling, freezing, ethanol, H2O2, permanganate, iodine, ethylene oxide vapour, detergents,

organic solvents, formaldehyde, UV and gamma irradiation, and standard autoclaving.

Since conventional methods of sterilisation and disinfection do not decontaminate the CJD

infectious agent, specific measures must be used, however, many of these are impractical in the

dental practice.

Although the TSE agent is known to be infectious it is not contagious in the usual sense.

Individuals exposed to patients with CJD: their spouses, nurses and doctors, do not appear to

have an increased risk of developing the disease. Furthermore, professionals who might be

considered 'high risk' in relation to exposure to TSE agents: e.g. pathologists, neurosurgeons,

butchers etc. also do not appear to be at an increased risk of developing CJD. No proven instance

of CJD contracted occupationally has yet been identified. However, over 170 cases of iatrogenic

CJD contracted through inoculation of contaminated CNS tissue or corneal transplantation serve

to remind those of us involved in the management of all CJD patients of the importance of safety

procedures in relation to the TSE agents.



Date: January 18, 2007 at 8:32 am PST

Fourth case of transfusion-associated vCJD infection in the United Kingdom

Editorial team (, Eurosurveillance editorial office

A suspected case of variant Creutzfeldt-Jakob disease (vCJD) has recently been diagnosed
in a patient in the United Kingdom (UK), who received a blood transfusion from a donor who
later developed vCJD [1]. This is the fourth case of probable transfusion transmission of
vCJD infection in the UK. Three of the four recipients developed symptoms of vCJD.
The first symptomatic case of vCJD associated with blood transfusion was identified in
December 2003. This individual developed vCJD six and a half years after transfusion of
red cells donated by an individual who developed symptoms of vCJD three and a half years
after donation.

A second case of vCJD 'infection' was identified a few months later in a person who had
received red cells from a donor who developed symptoms of vCJD 18 months after donation.
This patient (the second case) died from causes unrelated to vCJD five years after
transfusion. Post-mortem investigations found abnormal prion protein in the spleen
and a cervical lymph node., However, prion protein was not found in the brain, and no
pathological features of vCJD were found.

A third case developed symptoms of vCJD six years after receiving a transfusion of red
blood cells, and died two years and eight months later. The donor of the blood involved
developed vCJD about 20 months after donating it.

These three cases have been published as case reports and in the findings of the ongoing
collaborative study between the National Blood Services, the National CJD Surveillance Unit,
and the Office for National Statistics. This study aims to collect evidence about transmission
of CJD or vCJD via the blood supply [2,3,4,5].

The new, fourth case is in a patient who developed symptoms of vCJD eight and a half years
after receiving a transfusion of red blood cells from a donor who developed vCJD about 17
months after this blood was donated [1]. The donor to this case also donated the vCJD-implicated
blood transfused to the third case. As for all other reported clinical vCJD cases that have been
tested for genotype, this patient is a methionine homozygote at codon 129 of the prion protein gene.
The patient is currently alive.

All four cases had received transfusions of non-leucodepleted red blood cells between 1996 and 1999.
Since October 1999, leucocytes have been removed from all blood used for transfusion in the UK. The
effect of leucodepletion on the reduction of the risk of transmission of vCJD from an infective
donation is uncertain.

This fourth case of vCJD infection associated with blood transfusion further increases the level of
concern about the risk of vCJD transmission between humans by blood transfusion, although much
remains unknown. This reinforces the importance of the existing precautions that have been introduced
to reduce the risk of transmission of vCJD infection by blood and blood products [6]. No cases of
vCJD have been associated with fractionated plasma products. The small group of living recipients
of vCJD-implicated blood transfusion in the UK have been informed of their potential exposure to
vCJD by blood transfusion, asked to take certain precautions to reduce the risk of onward
person-to-person transmission of vCJD during health care, and offered specialist neurological
evaluation and advice.

This article has been adapted from reference 1




Diagnosis and Reporting of Creutzfeldt-Jakob Disease
Singeltary, Sr et al.
JAMA.2001; 285: 733-734.


MARCH 26, 2003

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

disease in the United States

Email Terry S. Singeltary:

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?

Diagnosis and Reporting of Creutzfeldt-Jakob Disease

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





Terry S. Singeltary Sr.
P.O. Box 42
Bacliff, Texas USA 77518

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