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From: TSS ()
Subject: Extraneural Prion Neuroinvasion without Lymphoreticular System Infection
Date: September 1, 2005 at 7:51 am PST

Journal of Virology, September 2005, p. 11858-11863, Vol. 79, No. 18
0022-538X/05/$08.00+0 doi:10.1128/JVI.79.18.11858-11863.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Extraneural Prion Neuroinvasion without Lymphoreticular System Infection
Jason C. Bartz,1 Crista DeJoia,2 Tammy Tucker,2 Anthony E. Kincaid,3 and Richard A. Bessen2*
Department of Medical Microbiology & Immunology,1 Department of Physical Therapy, Creighton University, Omaha, Nebraska 68178,3 Department of Veterinary Molecular Biology, Montana State University, Bozeman, Montana 597172

Received 23 March 2005/ Accepted 22 June 2005

While prion infection of the lymphoreticular system (LRS) is necessary for neuroinvasion in many prion diseases, in bovine spongiform encephalopathy and atypical cases of sheep scrapie there is evidence to challenge that LRS infection is required for neuroinvasion. Here we investigated the role of prion infection of LRS tissues in neuroinvasion following extraneural inoculation with the HY and DY strains of the transmissible mink encephalopathy (TME) agent. DY TME agent infectivity was not detected in spleen or lymph nodes following intraperitoneal inoculation and clinical disease was not observed following inoculation into the peritoneum or lymph nodes, or after oral ingestion. In contrast, inoculation of the HY TME agent by each of these peripheral routes resulted in replication in the spleen and lymph nodes and induced clinical disease. To clarify the role of the LRS in neuroinvasion, the HY and DY TME agents were also inoculated into the tongue because it is densely innervated and lesions on the tongue, which are common in ruminants, increase the susceptibility of hamsters to experimental prion disease. Following intratongue inoculation, the DY TME agent caused prion disease and was detected in both the tongue and brainstem nuclei that innervate the tongue, but the prion protein PrPSc was not detected in the spleen or lymph nodes. These findings indicate that the DY TME agent can spread from the tongue to the brain along cranial nerves and neuroinvasion does not require agent replication in the LRS. These studies provide support for prion neuroinvasion from highly innervated peripheral tissues in the absence of LRS infection in natural prion diseases of livestock.


* Corresponding author. Mailing address: Department of Veterinary Molecular Biology, P. O. Box 173610, Montana State University, Bozeman, MT 59717. Phone: (406) 994-1563. Fax: (406) 994-4303. E-mail:


Journal of Virology, September 2005, p. 11858-11863, Vol. 79, No. 18
0022-538X/05/$08.00+0 doi:10.1128/JVI.79.18.11858-11863.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.


seems like this might implicate a potential source via infectivity and transmission via the oral surgical/dental route. also, makes the USA exporting of BOVINE TONGUE a risky business. ...


U.S. Domestic Exports: December 2004 and 2004 Year-to-Date,
not Seasonally Adjusted

(FAS Value, in Thousands of Dollars)
(Units of Quantity: Kilogram) December 2004 2004, through December
Quantity Value Quantity Value
.World 432,185 755 3,479,807 6,127
Bangladesh 23,623 38 47,380 77
Honduras 15,163 28 17,105 31
Hong Kong 0 0 47,151 86
Indonesia 0 0 83,245 193
Japan 0 0 25,697 57
Kazakhstan 0 0 145,001 175
Mexico 368,562 638 3,046,441 5,384
Nicaragua 6,537 13 6,537 13
Philippines 18,300 38 61,250 111

-------- Original Message --------
Subject: Presentation of a case of variant CJD in general dental practice [FULL TEXT]
Date: Tue, 27 Jul 2004 09:31:30 -0500
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy

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



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
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
Refereed Paper
Received 13.10.03; Accepted 16.01.04
© British Dental Journal 2004; 197: 7576


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
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.


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
? 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.




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


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

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

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

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


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:
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-
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.



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Evidence For CJD/TSE Transmission Via Dental Instruments


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