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From: TSS ()
Subject: MULE-DEER PLAGUED BY BLINDNESS AND CWD
Date: September 8, 2006 at 8:35 am PST

MULE-DEER PLAGUED BY BLINDNESS

One of Dr. Williams' last cases was an unusual cause of blindness in a mule deer. She was presented with the carcass of a recently shot adult male mule deer. Hunters east of Laramie noticed that the animal was blind and stumbling into trees and bushes. The major gross change was severe inflammation of both eyes, primarily keratitis and uveitis. Histologically the uveal tract and anterior and posterior chambers contained large colonies of coccobacilli, with associated necrosis.

Dr. Mills' laboratory isolated Yersinia pestis in pure culture from the media of the eye and from conjunctival sac. Other lesions in the deer were severe necrotizing nephritis, adrenalitis and lymphadentitis. The organisms in tissues stained immunohistochemically for antigens of Y. pestis. The deer was beyond unlucky, since it also tested positive for chronic wasting disease ("every animal is entitled to two diseases" - Dr. Stuart Young). CWD was probably incidental since the animal was in excellent nutritional condition. No lesions were present in brain.

Plague is unusual in big game since ungulates are considered resistant. There is a published report of plague in a free-ranging mule deer in Wyoming,1 an unpublished, laboratory-confirmed case in a mule deer in Montana,2 and bilateral plague-associated necrotizing panophthalmitis in a black-tailed deer in California.3 Ocular plague has been seen in Colorado (Dr. M. Miller, Colorado Division of Wildlife, unpublished observations; see image). As an aside, ocular plague also occurs rarely in people.4

Plague panophthalmitis in a mule deer. The image on the left shows buphthalmos with exudation. The image on the right shows the sagittally sectioned globe with exudatesin the anterior chamber and vitreous. Both images courtesy of Dr. Mike Miller, Colorado Division of Wildlife

If you are presented with a deer that is blind and hunters ask you if it is safe to eat, bear in mind the possibility that it may be plague. Leviticus had it right: we should not eat sick animals. Dr. Williams' graduate student, Dave Edmunds, will present this case at the annual meeting of the AAVLD this November.

Donal O'Toole/Beth Williams

1. Thorne E. T., Quan, T.J., Williams, E. S., Walthall, T.J., Daniels, D.: 1987, Plague in a free-ranging mule deer from Wyoming. J Wildl Dis 23(1): 155 - 159

2. http://archives.foodsafetynetwork.ca/animalnet/2003/9 2003/animalnet_september_12.htm#PLAGUE

3. Jessup, D. A.; Murphy, C. J.; Kock, N.; Jang, S.; Hoefler, L

Ocular lesions of plague (Yersinia pestis) in a black-tailed deer (Odocoileus hemionus columbianus) Journal of Zoo and Wildlife Medicine 20 (3), 1989 p.360-363.

4. Carter, D. B., Ellis, P. P.: 1987, Yersinia pestis endophthalmitis. Am J Ophthalmol 103 (5): 721 - 722.

http://wyovet.uwyo.edu/Newsletters/Vol_6/Iss_3.pdf

Greetings,

I would kindly like to comment please ;

>>>Dr. Mills' laboratory isolated Yersinia pestis in pure culture from the media of the eye and from conjunctival sac. Other lesions in the deer were severe necrotizing nephritis, adrenalitis and lymphadentitis. The organisms in tissues stained immunohistochemically for antigens of Y. pestis. The deer was beyond unlucky, since it also tested positive for chronic wasting disease ("every animal is entitled to two diseases" - Dr. Stuart Young). CWD was probably incidental since the animal was in excellent nutritional condition. No lesions were present in brain. <<<

SOMETHING to ponder for sure, and that is, WAS CWD INCIDENTAL with the blindness of this animal??? it is not out of the relm of science for CWD or maybe even a different strain of TSE in deer and or elk to cause blindness, not to say that this is a case. WE have human strains of TSE that cause blindness i.e. Heidenhain Variant Creutzfeldt Jakob disease, so to rule out blindness as part of CWD in all cases would not be scientific without proper evidence in my opinion. ...TSS

NEUROLOGY 2006;67:531-533
© 2006 American Academy of Neurology

----------------------------------------------------------------------------
----
Brief Communications

The MM2-cortical form of sporadic Creutzfeldt–Jakob disease presenting with
visual disturbance
I. Nozaki, MD, T. Hamaguchi, MD, PhD, M. Noguchi-Shinohara, MD, K. Ono, MD,
PhD, H. Shirasaki, MD, K. Komai, MD, PhD, T. Kitamoto, MD, PhD and M.
Yamada, MD, PhD
From the Department of Neurology and Neurobiology of Aging (I.N., T.H.,
M.N.-S., K.O., K.K., M.Y.), Kanazawa University Graduate School of Medical
Science, Kanazawa; Department of Neurology (H.S.), Tonami General Hospital,
Tonami; and Department of Prion Protein Research, Division of CJD Science
and Technology (T.K.), Tohoku University Graduate School of Medicine,
Sendai, Japan.

Address correspondence and reprint requests to Dr. Ichiro Nozaki, Department
of Neurology and Neurobiology of Aging, Kanazawa University Graduate School
of Medical Science, 13-1 Takara-machi, Kanazawa, Ishikawa 920-8640, Japan;
e-mail: ichi51@med.kanazawa-u.ac.jp

A subclass of sporadic Creutzfeldt–Jakob disease (sCJD) characterized by
onset with visual symptoms (Heidenhain variant) has been reported to belong
to the MM1 or MV1 type according to Parchi's classification. The authors
report a 65-year-old woman with MM2-cortical sCJD with slowly progressive
visual disturbance as the initial symptom. Diffusion-weighted MRIs revealed
hyperintensity in both occipital cortices at an early stage.

http://www.neurology.org/cgi/content/abstract/67/3/531

A case of sporadic Creutzfeldt Jakob disease with anterior visual pathway
involvement

Mooney T1, Sreekumar J1, Hemanth S2, Mathuranath PS1, Sarada C1
1 Departments of Neurology, Sree Chitra Tirunal Institute for Medical
Sciences and Technology, Trivandrum - 695 011, India
2 Departments of Radiology, Sree Chitra Tirunal Institute for Medical
Sciences and Technology, Trivandrum - 695 011, India

Date of Acceptance 08-Nov-2004


snip...


Our patient started with progressive blindness followed over next ten months
by dementia and myoclonus. Other causes were ruled out by appropriate
investigations. CJD was considered initially though the optic neuropathy and
the absence of the characteristic EEG findings by ten months into the
illness raised questions. The subsequent evolution of dystonia, rigidity,
myoclonus, and the characteristic periodic complexes on EEG and posterior
thalamic hyperintensities on MRI, however, favor the diagnosis of sporadic
CJD.[3]

Anterior visual pathway involvement has so far been reported in only two
case reports in the literature. Kitagawa et al from Japan reported a patient
who had extensive and early brain atrophy on CT scan and whose post mortem
showed degeneration of the optic nerve as well as the cerebral and
cerebellar white matter.[4] Lesser et al reported a case of bilateral optic
atrophy confirmed at autopsy in whom features of optic atrophy were not
documented ante mortem.[5] Our case highlights the rare occurrence of the
anterior visual pathway involvement in sporadic CJD and demonstrates that it
can be the presenting feature, preceding the typical clinical or EEG
features of this disease by months.

http://www.neurologyindia.com/article.asp?issn=0028-3886;year=2005;volume=53;issue=1;spage=120;epage=121;aulast=Mooney

Case #388 Heidenhain variant of Creutzfeldt-Jakob Disease

http://www.uiowa.edu/~c064s01/nr388.htm

ARRUDA, Walter Oleschko, BORDIGNON, Kelly C., MILANO, Jerônimo B. et al.
Creutzfeldt-Jakob disease, Heidenhain variant: case report with MRI (DWI)
findings. Arq. Neuro-Psiquiatr., June 2004, vol.62, no.2a, p.347-352. ISSN
0004-282X.

http://www.scielo.br/scielo.php?pid=S0004-282X2004000200029&script=sci_abstract&tlng=en

Creutzfeldt-Jakob Disease Presenting with Visual Blurring, Diplopia and

Visual Loss: Heidenhain’s Variant

K E Lee,*MBBS, MRCP (UK), N K Loh,**MBBS, MRCP (UK), M Med (Int Med), A K Y
Tan,***FAMS, MBBS, MRCP (UK),

W L Lee,†

MBBS (Hons), MRCP (UK), M Med (Paed), H T L Tjia,‡

FAMS, MBBS, M Med (Int Med)

http://www.annals.edu.sg/pdf_nov98/leeke.pdf

Creutzfeldt-Jakob’s Disease – Case Report With Emphasis

on the Electroencephalographic Features

Patrícia Coral*,**, Francisco M. B. Germiniani*, Carlos E. Silvado*,**,***

Epicentro – Centro Integrado de Atendimento de Epilepsia, Curitiba, PR


Creutzfeldt-Jakob’s Disease – Case Report With Emphasis

on the Electroencephalographic Features

Patrícia Coral*,**, Francisco M. B. Germiniani*, Carlos E. Silvado*,**,***

Epicentro – Centro Integrado de Atendimento de Epilepsia, Curitiba, PR

ABSTRACT

Creuzfeldt-Jakob’s Disease is a rare neurodegenerative disorder that is included among the transmissible

spongiform encephalopathies. The clinical features are those of a rapid progressive dementia with mioclonic

jerks, which progresses to death in less than one year. We report the case of a 79 years old woman, with

initial complaints of vertigo, visual and gait compromise, with an initial brain MRI, EEG and CSF that had

no specific features of CJD. After 12 days she was again admitted to the hospital with a worsening of her

symptoms, along with global spasticity, inability to walk and a further deterioration of speech and swallowing.

A new EEG disclosed periodic triphasic complexes, typical of the disease. CSF had a positive 14-3-3 protein.

She later evolved with mioclonic jerks, coma, multiple infectious complications and, ultimately, death 45

days after her second admission. We focus on the role of the EEG as an adjuctive eletrophysiological tool for

the presumptive in vivo diagnosis of the disease.

Key words: dementia, Creutzfeldt-Jakob’s Disease, prion.

RESUMO

Doença de Creutzfeldt-Jakob – Relato de caso com enfoque nos aspectos eletrencefalográficos


http://www.epilepsia.org.br/epi2002/JEp189-92.pdf

[Docket No. FSIS-2006-0011] FSIS Harvard Risk Assessment of Bovine
Spongiform Encephalopathy (BSE)

http://www.fsis.usda.gov/OPPDE/Comments/2006-0011/2006-0011-1.pdf

TSS




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