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From: TSS ()
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 There is a published report of plague in a free-ranging mule deer in Wyoming,1 an unpublished, laboratory-confirmed case in a mule deer in Montana,2 and bilateral plague-associated necrotizing panophthalmitis in a black-tailed deer in California.3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 M. Miller, Colorado Division of Wildlife, unpublished observations; see image).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 ---------------------------------------------------------------------------- The MM2-cortical form of sporadic Creutzfeldt–Jakob disease presenting with Address correspondence and reprint requests to Dr. Ichiro Nozaki, Department A subclass of sporadic Creutzfeldt–Jakob disease (sCJD) characterized by http://www.neurology.org/cgi/content/abstract/67/3/531 A case of sporadic Creutzfeldt Jakob disease with anterior visual pathway Mooney T1, Sreekumar J1, Hemanth S2, Mathuranath PS1, Sarada C1 Date of Acceptance 08-Nov-2004 Anterior visual pathway involvement has so far been reported in only two 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. 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 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 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 [Docket No. FSIS-2006-0011] FSIS Harvard Risk Assessment of Bovine http://www.fsis.usda.gov/OPPDE/Comments/2006-0011/2006-0011-1.pdf TSS
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