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From: TSS ()
Subject: Re: Information for dentists about the management of patient s with, or ‘atrisk’ of, Creutzfeldt-Jakob Disease (CJD) including variant CJD (vCJD)
Date: July 26, 2005 at 6:13 am PST

CDC
Morbidity and Mortality Weekly Report
Recommendations and Reports December 19, 2003 / Vol. 52 / No. RR-17

Guidelines for Infection Control
in Dental Health-Care Settings — 2003

36 MMWR December 19, 2003
Creutzfeldt-Jakob Disease and Other
Prion Diseases
Creutzfeldt-Jakob disease (CJD) belongs to a group of rapidly
progressive, invariably fatal, degenerative neurological disorders,
transmissible spongiform encephalopathies (TSEs) that
affect both humans and animals and are thought to be caused
by infection with an unusual pathogen called a prion. Prions
are isoforms of a normal protein, capable of self-propagation
although they lack nucleic acid. Prion diseases have an incubation
period of years and are usually fatal within 1 year of
diagnosis.
Among humans, TSEs include CJD, Gerstmann-Straussler-
Scheinker syndrome, fatal familial insomnia, kuru, and variant
CJD (vCJD). Occurring in sporadic, familial, and acquired
(i.e., iatrogenic) forms, CJD has an annual incidence in the
United States and other countries of approximately 1 case/
million population (445–448). In approximately 85% of
affected patients, CJD occurs as a sporadic disease with no
recognizable pattern of transmission. A smaller proportion of
patients (5%–15%) experience familial CJD because of inherited
mutations of the prion protein gene (448).
vCJD is distinguishable clinically and neuropathologically
from classic CJD, and strong epidemiologic and laboratory
evidence indicates a causal relationship with bovine spongiform
encephalopathy (BSE), a progressive neurological disorder of
cattle commonly known as mad cow disease (449–451). vCJD,
was reported first in the United Kingdom in 1996 (449) and
subsequently in other European countries (452). Only one
case of vCJD has been reported in the United States, in an
immigrant from the United Kingdom (453). Compared with
CJD patients, those with vCJD are younger (28 years versus
68 years median age at death), and have a longer duration of
illness (13 months versus 4.5 months). Also, vCJD patients
characteristically exhibit sensory and psychiatric symptoms that
are uncommon with CJD. Another difference includes the ease
with which the presence of prions is consistently demonstrated
in lymphoreticular tissues (e.g., tonsil) in vCJD patients by
immunohistochemistry (454).
CJD and vCJD are transmissible diseases, but not through
the air or casual contact. All known cases of iatrogenic CJD
have resulted from exposure to infected central nervous tissue
(e.g., brain and dura mater), pituitary, or eye tissue. Studies in
experimental animals have determined that other tissues have
low or no detectable infectivity (243,455,456). Limited
experimental studies have demonstrated that scrapie (a TSE in
sheep) can be transmitted to healthy hamsters and mice by
exposing oral tissues to infectious homogenate (457,458).
These animal models and experimental designs might not be
directly applicable to human transmission and clinical dentistry,
but they indicate a theoretical risk of transmitting prion
diseases through perioral exposures.
According to published reports, iatrogenic transmission of
CJD has occurred in humans under three circumstances: after
use of contaminated electroencephalography depth electrodes
and neurosurgical equipment (459); after use of extracted
pituitary hormones (460,461); and after implant of contaminated
corneal (462) and dura mater grafts (463,464) from
humans. The equipment-related cases occurred before the routine
implementation of sterilization procedures used in healthcare
facilities.
Case-control studies have found no evidence that dental
procedures increase the risk of iatrogenic transmission of TSEs
among humans. In these studies, CJD transmission was not
associated with dental procedures (e.g., root canals or extractions),
with convincing evidence of prion detection in human
blood, saliva, or oral tissues, or with DHCP becoming occupationally
infected with CJD (465–467). In 2000, prions were
not found in the dental pulps of eight patients with
neuropathologically confirmed sporadic CJD by using electrophoresis
and a Western blot technique (468).
Prions exhibit unusual resistance to conventional chemical
and physical decontamination procedures. Considering this
resistance and the invariably fatal outcome of CJD, procedures
for disinfecting and sterilizing instruments potentially contaminated
with the CJD prion have been controversial for years.
Scientific data indicate the risk, if any, of sporadic CJD transmission
during dental and oral surgical procedures is low to
nil. Until additional information exists regarding the transmissibility
of CJD or vCJD, special precautions in addition to
Vol. 52 / RR-17 Recommendations and Reports 37
standard precautions might be indicated when treating known
CJD or vCJD patients; the following list of precautions is provided
for consideration without recommendation
(243,249,277,469):
• Use single-use disposable items and equipment whenever
possible.
• Consider items difficult to clean (e.g., endodontic files,
broaches, and carbide and diamond burs) as single-use
disposables and discard after one use.
• To minimize drying of tissues and body fluids on a device,
keep the instrument moist until cleaned and decontaminated.
• Clean instruments thoroughly and steam-autoclave at 134ºC
for 18 minutes. This is the least stringent of sterilization
methods offered by the World Health Organization. The
complete list (469) is available at http://www.who.int/emcdocuments/
tse/whocdscsraph2003c.html.
• Do not use flash sterilization for processing instruments
or devices.
Potential infectivity of oral tissues in CJD or vCJD patients is
an unresolved concern. CDC maintains an active surveillance
program on CJD. Additional information and resources are
available at http://www.cdc.gov/ncidod/diseases/cjd/cjd.htm.

snip...

http://www.ada.org/prof/resources/topics/cdc/guidelines_cdc_infection.pdf

PRACTICE

BRITISH DENTAL JOURNAL VOLUME 197 NO. 2 JULY 24 2004 75

Presentation of a case of variant CJD in general
dental practice

A. J. Smith1, D. I. Russell2, J. Greene3, A. Lowman4 and J. W. Ironside5

This case report describes the initial presentation of variant CJD to a
general
dental practitioner. The case highlights the importance of prompt
referral of
patients presenting with a history of atypical facial symptoms.

1Senior Lecturer, Microbiology, Glasgow Dental Hospital &
School; 2Consultant Oral & Maxillofacial Surgeon, Glasgow
Dental Hospital & School; 3Consultant Neurologist,
Institute of Neurological Sciences, Southern General
Hospital, Glasgow; 4Registrar in Neurology, National CJD
Surveillance Unit, University of Edinburgh, Western
General Hospital, Edinburgh; 5Professor of Clinical
Neuropathology, National CJD Surveillance Unit, University
of Edinburgh, Western General Hospital, Edinburgh
Correspondence to: A. J. Smith, Infection Research Group,
Glasgow Dental Hospital & School, 378 Sauchiehall Street,
Glasgow G2 3JZ, Scotland
Email: a.smith@dental.gla.ac.uk
Refereed Paper
doi:10.1038/sj.bdj.4811468
Received 13.10.03; Accepted 16.01.04
© British Dental Journal 2004; 197: 7576

CASE REPORT

A 28-year-old patient presented to their
general dental practitioner with a 4-week
history of paraesthesia of the left side of
the face including the lower lip. The
patient was referred for an oral surgery
consultant clinic appointment for a more
detailed appraisal of the patients signs
and symptoms.
Examination at the consultant clinic
revealed an unremarkable past dental and
medical history. The patient complained of
a pins and needles sensation in the left
cheek, left lower lip and chin and the skin
of the left hand. Extra-oral examination
demonstrated a partial loss of sensation as
demonstrated by an impaired response to
pin prick and light touch, as well as two
point discrimination. This was evident in
the areas of the left face supplied by the
infra-orbital and mental nerves and the
palm and back of the hand (C6, C7, C8).
There was no weakness of the facial muscles
and the right side was unaffected.
Intra-oral examination revealed a healthy
intact dentition with no obvious signs of
dental disease. Due to the unusual distribution
of the sensory abnormalities the
patient was referred for an urgent neurological
examination.
On presentation to the neurology clinic
for a detailed neurological examination,
3 months after initial presentation to the
dental practitioner, some change in the
patients personality were noted. These
included becoming increasingly withdrawn
with episodes of confusion. Clinical
examination revealed that the patient's
sensory impairment on the left side had
extended to include the left arm, leg and
trunk. No other neurological signs and
symptoms were observed. Approximately
1 month later further diagnostic tests were
performed as follows:

" EEG  mild diffuse slowing
" MRI brain scan  bilateral diffuse areas
of signal hypersensitivity affecting the
pulvinar region of the brain
" CSF  14-3-3 protein negative
" CSF  white cell count normal

On the basis of the clinical presentation
of the sensory symptoms, psychiatric features
and the MRI results a diagnosis of
probable variant CJD was made. Eight
months after presentation to the dental
practitioner the patient died and the clinical
diagnosis of variant CJD was confirmed
following autopsy.

DISCUSSION

Psychiatric symptoms are common in the
early stages of vCJD. Typical presentations
are depression, anxiety and behavioural
change.1 Neurological symptoms such as
pain, paraesthesia and numbness precede
psychiatric symptoms in 15% of cases and
are present in combination with psychiatric
symptoms in 22% of cases from the onset
of disease. The most common early neurological
(< 4 months onset) features are persistent
pain affecting the limbs, trunk and
face but not associated with sensory symptoms.
Within 46 months of onset paraes-

? A description of a patient presenting with vCJD to a general dental
practitioner.
? vCJD can present with atypical facial symptons such as paraesthesia.
? The case highlights the importance of medical history taking at each
visit and the prompt
referral of any patients with atypical signs and symptoms.

I N B R I E F

PRACTICE

76 BRITISH DENTAL JOURNAL VOLUME 197 NO. 2 JULY 24 2004

thesia and numbness in a similar distribution
to, and often associated with pain is
common.2,3 A diagnosis of CJD has been
confirmed following autopsy in all cases
where a post-mortem examination has
been performed.4

DIAGNOSIS OF VCJD

An ante-mortem diagnosis of vCJD can be
difficult in the early stages of the disease.
However, diagnosis can be facilitated by
use of a number of diagnostic criteria based
on a detailed clinical history of the nature
of the symptoms, pattern of progression
and duration of the illness and diagnostic
tests, and can lead to a clinical diagnosis
with a high degree of accuracy.4 A number
of tests and investigations can contribute
to a diagnosis:

1. Blood tests
In addition to excluding other forms of illness,
blood tests collected with informed
consent can be performed for any of the
genetic mutations already identifiable in
inherited prion diseases. Blood can also be
tested for genetic susceptibility to vCJD by
detecting the presence of methionine/
methionine homozygosity at codon 129. To
date, all cases of vCJD are homozygous for
methionine at this location.

2. EEG
This can be a useful test for the diagnosis of
sporadic CJD. In other forms of CJD the
EEG may be normal or there may be nonspecific
abnormalities.

3.Cranial MRI
An MRI scan can be useful in assisting a
diagnosis. In vCJD, abnormal changes can
be observed in the posterior thalamic area
of the brain (pulvinar sign) and in sCJD
there are occasional changes in the basal
ganglia.5

4. CSF
Analysis of CSF is useful to exclude some
types of infection. An increase in the neuronal
protein 14-3-3 in the CSF can be of
considerable help in the diagnosis of sCJD,
but it is less helpful in vCJD.6

5. BIOPSY
Brain biopsy is not recommended for any
form of CJD unless an alternative treatable
condition is suspected in the differential
diagnosis. In vCJD, PrPSc also accumulates
outside of the CNS in lymphoid tissues, so
that biopsy of tonsillar tissue can provide a
means of a probable diagnosis of vCJD.
Within the UK, the use of tonsil biopsy for
diagnosis of vCJD has been developed and
validated.7

CONCLUSION

Although sensory disturbances in one or
more divisions of the fifth cranial nerve is a
rare presentation for vCJD, this possibility
should be considered, particularly if the
sensory symptoms progress to other areas.
Some of the early clinical features of vCJD
such as personality change, loss of concentration
or sensory symptoms may occur in
psychiatric conditions (sometimes as side
effects of psychotropic drugs), or in the
early stages of multiple sclerosis, However,
the persistence of these symptoms over a
number of weeks with no apparent cause
should alert the practitioner to the presence
of a more serious underlying cause and
urgent referral for further investigation
should be instituted. In particular, the
emergence of ataxia (unsteady gait),
myoclonus (sudden muscle spasms) or
other movement disorders should strongly
alert the clinician to suspect a progressive
neurodegenerative condition such as vCJD.
The authors wish to acknowledge the kind support of
the patient's family to allow us the opportunity to
publish this report.

1. Spencer M D, Knight R S G, Will R G. First hundred
cases of variant CJD: retrospective case note review
of early psychiatric and neurological features. Br Med
J 2002; 324: 1479-1482.
2. Henry C, Knight R. Clinical features of variant
Creutzfeldt-Jakob disease. Rev Med Virol 2002; 12:
143-150.
3. Macleod M A, Knight R, Stewart G, Zeidler M, Will R.
Sensory features of variant Creutzfeldt-Jakob disease.
J Neurol Neurosurg Psychiatry 2000; 69: 413-414.
4. Will R G, Zeidler M, Stewart G E et al. Diagnosis of new
variant Creutzfeldt-Jakob disease. Annals of
Neurology 2000; 47: 575-582.
5. Zeidler M, Sellar R J, Collier D A et al. The pulvinar sign
on magnetic resonance imaging in variant
Creutzfeldt-Jakob disease. Lancet 2000; 355: 1412-
1418.
6. Hsich G, Kennedy K, Gibbs C J, Lee K H, Harrington M
G. The 14-3-3 brain protein in cerebrospinal fluid as a
marker for transmissible spongiform
encephalopathies. N Engl J Med 1996; 335: 924-930.
7. Hill A F, Butterworth R J, Joiner S et al. Investigation of
variant Creutzfeldt-Jakob disease and other human
prion diseases with tonsil biopsy samples. Lancet
1999; 353: 183-189.

BRITISH DENTAL JOURNAL VOLUME 197 NO. 2 JULY 24, 2004

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15272338

Evidence For CJD/TSE Transmission Via Dental Instruments

From Terry S. Singletary, Sr
flounder@wt.net
1-24-3

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. a.smith@dental.gla.ac.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]

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12144804&dopt=Abstract

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

http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10580068&dopt=Abstract

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

Abstract

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

Introduction

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:

http://www.pnas.org/cgi/content/full/97/7/3418

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...

CJD/TSEs MUST BE MADE REPORTABLE NATIONALLY, SUPPORTED WITH A CJD QUESTIONNAIRE TO EVERY VICTIM/FAMILY THAT ASK REAL QUESTIONS PERTAINING TO ROUTE/SOURCE...TSS

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

http://jama.ama-assn.org/issues/v285n6/ffull/jlt0214-2.html

kind regards, terry

http://www.rense.com/general34/evi.htm

----- Original Message -----
From: "Terry S. Singeltary Sr."
To:
Sent: Tuesday, July 26, 2005 8:00 AM
Subject: Information for dentists about the management of patient s with, or ‘atrisk’ of, Creutzfeldt-Jakob Dis ease (CJD) including variant CJD (vCJD)

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

Gateway Approval Reference Number: 4463

Professor Raman Bedi

Chief Dental Officer – England

Room 332 Wellington House

133-135 Waterloo Road

London

SE1 8UG

Direct Line: 020 7 972 3995

Fax: 020 7972 3999

E-mail: raman.bedi@dh.gsi.gov.uk

4 February 2005

Dear Colleague

Information for dentists about the management of patients with, or ‘atrisk’

of, Creutzfeldt-Jakob Disease (CJD) including variant CJD (vCJD)

The aim of this letter is to clarify the situation with respect to the Primary

Dental Care of patients who have been diagnosed with CJD, or identified as

‘at-risk’ of CJD for public health purposes.

The clinical care – including dental care - of these patients, should not be

compromised in any way. As for all patients, satisfactory standards of

decontamination are required. Should dental treatment progress to head and

neck surgery, special precautionary measures may need to be taken to

reduce any possible transmission of CJD.

The possibility that CJD may be spread from patient to patient in healthcare

settings arises from knowledge that the CJD agent can be detected in certain

tissues, and that any infectivity transferred on instruments in the course of

their use may not be entirely removed (nor inactivated) by normal

decontamination processes.

Information about the appropriate management of these patients’ dental

treatment is summarised below. The Annex (Annex A) attached to this letter

provides supporting information and sources for further information.

KEY MESSAGES

Please ensure that:

- Patients with CJD, or identified as ‘at-risk’ of CJD for public health

purposes, (or their relatives) are not refused routine dental treatment

- Satisfactory standards of decontamination are observed

Gateway Approval Reference Number: 4463

- Information about patients who are ‘at-risk’ of CJD is included in any

referrals for surgery, and recorded in your records.

Actions for all Primary Dental Carers

When treating a patient with CJD, or a patient who informs you that he/she

has been identified as ‘at-risk’ of CJD, you should:

• Ensure that satisfactory standards of decontamination are observed.

Under these conditions, routine dentistry is understood to be low-risk, and

therefore no special infection control precautions are advised for the

instruments used on symptomatic or ‘at-risk’ patients.

The recommendations of the British Dental Association1 should be

followed at all times, and for all patients.

Further information on infection control procedures specifically for patients

with CJD or ‘at-risk’ of CJD is available in the guidance developed by the

Advisory Committee on Dangerous Pathogens (ACDP) Transmissible

Spongiform Encephalopathy (TSE) Working Group, Transmissible

spongiform encephalopathy agents: safe working and the prevention of

infection2.

For a patient who informs you that he/she has been identified as ‘at-risk’ of

CJD, you should also:

• Ensure that information about the patient’s ‘at-risk’ status is included

in any referrals for surgery. Head and neck surgery may involve contact

with tissues of high or medium infectivity, for which special infection control

precautions are advised. Please also record this information in your

records for this patient.

PROFESSOR RAMAN BEDI

Chief Dental Officer – England

Gateway Approval Reference Number: 4463

References

1 British Dental Association (February 2003) Advice sheet A12 Infection

Control in Dentistry http://www.bda-dentistry.org.uk/advice/docs/A12.pdf

2 Transmissible spongiform encephalopathy agents: safe working and the

prevention of infection. Guidance from the Advisory Committee on

Dangerous Pathogens and the Spongiform Encephalopathy Advisory

Committee. 1998, 2003 and 2004

http://www.advisorybodies.doh.gov.uk/acdp/tseguidance/

ANNEX A

Further information on managements of patients with, or at

risk of, CJD in Primary Dental Care

1. Categories of patients for whom this information applies

Details of the classification of patients with symptomatic CJD disease and

patients who are considered ‘at risk’ of CJD while asymptomatic can be found

in Table 4a of the guidance developed by the Advisory Committee on

Dangerous Pathogens (ACDP) Transmissible Spongiform Encephalopathy

(TSE) Working Group, Transmissible spongiform encephalopathy agents:

safe working and the prevention of infection2. This table is reproduced below.

Table 4a of TSE Infection Control Guidelines: Categorisation of patients by risk

1. Symptomatic patients 1.1 Patients who fulfil the diagnostic criteria for definite,

probable or possible CJD or vCJD (see Annex B for

diagnostic criteria).

1.2 Patients with neurological disease of unknown

aetiology who do not fit the criteria for possible CJD or

vCJD, but where the diagnosis of CJD is being actively

considered

2. Asymptomatic patients at risk from familial forms of

CJD linked to genetic mutations

2.1 Individuals who have or have had two or more blood

relatives affected by CJD or other prion disease, or a

relative known to have a genetic mutation indicative of

familial CJD.

2.2 Individuals who have been shown by specific

genetic testing to be at significant risk of developing

CJD or other prion disease.

3. Asymptomatic patients potentially at risk from

iatrogenic exposure##

3.1 Recipients of hormone derived from human pituitary

glands, e.g. growth hormone, gonadotrophin.

3.2 Individuals who have received a graft of dura mater.

(People who underwent neurosurgical procedures or

operations for a tumour or cyst of the spine before

August 1992 may have received a graft of dura mater,

and should be treated as at risk, unless evidence can be

provided that dura mater was not used).

3.3 Patients who have been contacted as potentially at

risk because of exposure to instruments used on, or

receipt of blood, plasma derivatives, organs or tissues

donated by, a patient who went on to develop CJD or

vCJD*.

## NB: A decision on the inclusion of corneal graft recipients in the "iatrogenic at risk" category is

pending completion of a risk assessment.

* The CJD Incidents Panel, which gives advice to the local team on what action needs to be taken when

a patient who is diagnosed as having CJD or vCJD underwent surgery or donated blood, organs or

tissues before CJD/vCJD was identified, will identify contacts who are potentially at risk.

- 1 -

ANNEX A

- 2 -

2. Dentistry in the TSE Infection Control Guidelines2

Part 4, page 16 of this guidance states that:

"The risks of transmission of infection from dental instruments are

thought to be very low provided optimal standards of infection control and

decontamination are maintained. General advice on the decontamination

of dental instruments can be found in guidance prepared by the British

Dental Association (BDA) on ‘Infection control in dentistry’2. This

document (known as the ‘A12’) is available from the BDA and can be

accessed on their website at www.bda-dentistry.org.uk. Dental

instruments used on patients defined in Table 4a can be handled in the

same way as those used in any other low risk surgery i.e. these

instruments can be reprocessed according to best practice and returned to

use. Optimal reprocessing standards must be observed. Additionally,

dentists are reminded that any instruments labelled by manufacturers as

‘single use’ should not be re-used under any circumstances.

"There is no reason why any of the categories of patients defined in

Table 4a or their relatives should be refused routine dental treatment.

They can be treated in the same way as any member of the general

public."

3. Tissues of high or medium infectivity for CJD and vCJD

In sporadic (and familial) CJD, significant infectivity is assumed to exist in the

central nervous system, olfactory epithelium and eye.

In variant CJD, significant infectivity is assumed to exist in these same tissues

and also in gastrointestinal lymphoid tissue and peripheral lymphoid tissue.

When patients ‘at-risk’ of CJD/vCJD undergo maxillio-facial surgery that may

disrupt certain cranial nerves, or lymphoid tissues of the head and neck,

special infection control precautions may need to be taken, as described in

the TSE Infection Control Guidance2.

4. Patients identified as ‘at-risk’ of CJD for public health purposes

There are several groups of patients who are identified as being at an

additional risk of CJD (i.e. a risk over and above the risk in the general UK

population that is around 1 in a million for sporadic CJD and is currently

unknown for vCJD). These patients are considered ‘at-risk’ of CJD for public

health purposes.

Over the past year, there has been a considerable increase in the number of

patients classified as ‘at-risk’ of vCJD due to the notification of patients

considered at risk due to receipt of UK blood products. This number may

increase further if more blood donors develop vCJD.

ANNEX A

- 3 -

Patients identified as ‘at-risk’ of CJD (including vCJD) for public health

purposes are asked to take the following precautions to reduce any possible

risk of spreading CJD:

Not to donate blood, organs or tissues

To inform healthcare staff before they undergo medical, surgical or dental

treatment

To inform their families in case they need emergency surgery in the future.

The health care professionals who notify these patients of their ‘at-risk’ status

have been asked to arrange for the information to be recorded in patients’

hospital medical records and/or primary care notes.

The responsibility for informing Primary Dental Carers lies with the patients

themselves.

5. The risk of vCJD transmission during dentistry

In 2003 a study was undertaken to assess the risk of transmitting vCJD

through routine, or ‘high-street’, dentistry3. It was concluded that any risk of

vCJD transmission by routine dental procedures was ‘low’. (There is

evidence of vCJD infectivity in tonsillar tissue prior to the onset of symptoms,

and tonsils are considered a tissue of ‘medium-infectivity’. The possible risk

due to abrasion of the tonsils (particularly the lingual tonsils) was therefore

examined specifically: this risk appeared to be remote. The possibility of

infectivity in other tissues (e.g. dental pulp) was also explored, and even for

pessimistic scenarios, it was estimated that the risks of transmitting vCJD

would be low.)

Many inputs to this risk assessment are subject to large ranges of uncertainty.

It was noted that the findings might not apply if decontamination procedures

(involving cleaning and autoclaving) used in high-street dentistry are less

efficient than assumed.

As stated in the report:

"As for hospital surgery, the key consideration in minimising any risk of

transmission is assuring the efficiency of instrument decontamination, even

though current methods cannot remove such risks completely. In line with

SEAC [Spongiform Encephalopathy Advisory Committee] advice, potential

risks can be further reduced by introduction of more single-use instruments

where appropriate, especially for difficult-to-clean items."

6. Advice from the CJD Incidents Panel

Despite the low estimated risk, one of the recommendations of the CJD

Incidents Panel (the expert committee set up by the Chief Medical Officer in

2000 to advise hospitals, trusts and public health teams on how to manage

incidents involving possible transmission of CJD between patients) is that

patients inform their dentists of their ‘at-risk’ status. This is to enable Primary

ANNEX A

- 4 -

Dental Carers to take the two appropriate actions of a) ensuring satisfactory

standards of decontamination are observed, and b) ensuring information

about patients’ CJD status is included in any referrals for head and neck

surgery.

7. Sources of further information

The TSE Infection Control Guidance2 includes a review and summary of what

is known about the distribution of CJD/vCJD infectivity in human (and animal)

tissues.

Information relating specifically to patients identified as ‘at-risk’ of vCJD due to

receipt of plasma products – including background information on vCJD, the

assessment of risk, special public health precautions, infection control issues

for these patients, and where to find further advice - is available at

http://www.hpa.org.uk/infections/topics_az/cjd/blood_products.htm.

Information about the CJD Incidents Panel is available at

http://www.hpa.org.uk/infections/topics_az/cjd/incidents_panel.htm

Other information about CJD, and further links, can be found at

http://www.hpa.org.uk/infections/topics_az/cjd/menu.htm.

You may also contact your local infection control department for further

advice.

8. References

1 British Dental Association (February 2003) Advice sheet A12 Infection

Control in Dentistry http://www.bda-dentistry.org.uk/advice/docs/A12.pdf

2 Transmissible spongiform encephalopathy agents: safe working and the

prevention of infection. Guidance from the Advisory Committee on

Dangerous Pathogens and the Spongiform Encephalopathy Advisory

Committee. 1998, 2003 and 2004

http://www.advisorybodies.doh.gov.uk/acdp/tseguidance/

3 Department of Health (July 2003) Risk Assessment for vCJD and Dentistry

http://www.dh.gov.uk/PolicyAndGuidance/HealthAndSocialCareTopics/CJ

D/CJDGeneralInformation/CJDGeneralArticle/fs/en?CONTENT_ID=40324

09&chk=a%2BL/hP

http://www.dh.gov.uk/assetRoot/04/09/63/48/04096348.pdf

A12 Infection control.qxd (2003)

http://www.udp.org.uk/resources/bda-cross-infection.pdf

BMJ

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

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:
"'flounder@wt.net'"

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:

e.asante@ic.ac.uk (until 9/12/02)

New e-mail: e.asante@prion.ucl.ac.uk (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

> >> Differences in tissue distribution could require new regulations
> >> regarding specific risk material (SRM) removal.
> >
> >
> >
> >
>
> snip...end
>
> full text ;
>
> http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf
>
> It was, however, performed in the USA in 1979, when it was shown that
cattle
> inoculated with the scrapie agent endemic in the flock of Suffolk sheep at
> the United States Department of Agriculture in Mission, Texas, developed a
> TSE quite unlike BSE. 32 The findings of the initial transmission, though
> not of the clinical or neurohistological examination, were communicated in
> October 1988 to Dr Watson, Director of the CVL, following a visit by Dr
> Wrathall, one of the project leaders in the Pathology Department of the
CVL,
> to the United States Department of Agriculture. 33 The results were not
> published at this point, since the attempted transmission to mice from the
> experimental cow brain had been inconclusive. The results of the clinical
> and histological differences between scrapie-affected sheep and cattle
were
> published in 1995. Similar studies in which cattle were inoculated
> intracerebrally with scrapie inocula derived from a number of
> scrapie-affected sheep of different breeds and from different States, were
> carried out at the US National Animal Disease Centre. 34 The results,
> published in 1994, showed that this source of scrapie agent, though
> pathogenic for cattle, did not produce the same clinical signs of brain
> lesions characteristic of BSE.
>
> http://www.bseinquiry.gov.uk/report/volume2/chaptea3.htm
>
> Visit to USA ... info on BSE and Scrapie
>
> http://www.bseinquiry.gov.uk/files/yb/1988/10/00001001.pdf

SCRAPIE USA MONTHLY REPORT 2005

AS of March 31, 2005, there were 70 scrapie infected source flocks (Figure 3). There were 11 new infected and source flocks reported in March (Figure 4) with a total of 51 flocks reported for FY 2005 (Figure 5). The total infected and source flocks that have been released in FY 2005 are 39 (Figure 6), with 1 flock released in March. The ratio of infected and source flocks released to newly infected and source flocks for FY 2005 = 0.76 : 1. IN addition, as of March 31, 2005, 225 scrapie cases have been confirmed and reported by the National Veterinary Services Laboratories (NVSL), of which 53 were RSSS cases (Figure 7). This includes 57 newly confirmed cases in March 2005 (Figure 8). Fourteen cases of scrapie in goats have been reported since 1990 (Figure 9). The last goat cases was reported in January 2005. New infected flocks, source flocks, and flocks released or put on clean-up plans for FY 2005 are depicted in Figure 10. ...

FULL TEXT ;

http://www.aphis.usda.gov/vs/nahps/scrapie/monthly_report/monthly-report.html

WITH the MAY report, a scrapie case documented in a GOAT IN THE USA...TSS

SCRAPIE USA UPDATE MAY 2005

SCRAPIE has increased drastically since the report i posted in March 2005, with additional case in a goat;

SCRAPIE USA MONTHLY REPORT 2005

AS of March 31, 2005, there were 70 scrapie infected source flocks (Figure 3). There were 11 new infected and source flocks reported in March (Figure 4) with a total of 51 flocks reported for FY 2005 (Figure 5). The total infected and source flocks that have been released in FY 2005 are 39 (Figure 6), with 1 flock released in March. The ratio of infected and source flocks released to newly infected and source flocks for FY 2005 = 0.76 : 1. IN addition, as of March 31, 2005, 225 scrapie cases have been confirmed and reported by the National Veterinary Services Laboratories (NVSL), of which 53 were RSSS cases (Figure 7). This includes 57 newly confirmed cases in March 2005 (Figure 8). Fourteen cases of scrapie in goats have been reported since 1990 (Figure 9). The last goat cases was reported in January 2005. New infected flocks, source flocks, and flocks released or put on clean-up plans for FY 2005 are depicted in Figure 10. ...

FULL TEXT ;

http://www.aphis.usda.gov/vs/nahps/scrapie/monthly_report/monthly-report.html

CWD USA UPDATE

http://www.aphis.usda.gov/vs/nahps/cwd/cwd-distribution.html

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

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• Evidence For CJD/TSE Transmission Via Dental Instruments

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