# Disease Emergence and Resurgence: The Wildlife-Human Connection



## terry (Sep 13, 2002)

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


CJD WATCH MESSAGE BOARD
TSS
Disease Emergence and Resurgence: The Wildlife-Human Connect
Thu Mar 30, 2006 16:45
70.110.93.218




Disease Emergence and Resurgence: The Wildlife-Human Connection

The USGS National Wildlife Health Center is pleased to announce the publication of Circular 1285 -- Disease Emergence and Resurgence: The Wildlife-Human Connection. This book was prepared in cooperation with the U.S. Fish and Wildlife Service. Major funding support was provided by the U.S. Fish and Wildlife Service, Division of Federal Assistance, Administrative Grant No. AP95-017.

The book is available for download in Adobe pdf format. By downloading and printing each of these files, you can reproduce the entire Circular 1285. You will need to have Adobe Acrobat Reader installed on your system to read pdf files. (Adobe Acrobat Reader download site)

The complete book as a single zipped PDF is available here. The individual sections of the book are available below.






http://www.nwhc.usgs.gov/publications/disease_emergence/index.jsp



TABLE OF CONTENTS;



http://www.nwhc.usgs.gov/publications/disease_emergence/Front.pdf



Chapter 5

Is This Safe to Eat?

"A crust eaten in peace is better than a banquet attended by anxiety." (Aesop, 6th century B.C.)

"There is no love sincerer than the love of food." (George Bernard Shaw)





SNIP...



Brain abscesses are occasionally found by deer hunters, but these lesions do not pose a health threat for humans and should not result in disposal of the carcass. These abscesses are thought to result from invasion by skin-inhabiting bacteria. They are much more prevalent in males than females, often are associated with the antler pedicel, and generally occur following velvet shedding to shortly after the antlers are shed.20 Brain tissue from infected animals should be discarded. Even if not infected, brain should no longer be utilized in any foods because of the emergence of chronic wasting disease (see Prions, this chapter).





Prions



Prion diseases continue to be a relatively little understood yet heavily studied group of emerging infectious diseases. They include scrapie, a long existing sheep disease; bovine spongiform encephalopathy (BSE) of cattle; Creutzfeld-Jacob disease (CJD) and kuru of humans; a variant CJD (vCJD) associated with BSE that causes disease in humans; mink spongiform encephalopathy; and most recently chronic wasting disease (CWD) of deer and elk.30,31CWD is of great concern to hunters and game ranchers as it is ultimately fatal and affects several deer species (Fig. 5.28). Unlike the vCJD associated with BSE, no link has been found between CWD and disease in humans. However, because there are many unanswered questions about CWD, health officials advise against consuming meat from animals known to be infected with CWD. In addition, hunters should wear disposable gloves when field dressing deer or elk taken in areas where this disease is found and when deboning meat. The purpose for deboning is to remove associated neural tissue, the consumption of which is considered to be the primary pathway for exposure to prions. A separate knife, not the one used to butcher the deer, should be used to sever the spinal cord when the head is removed. This precaution avoids contamination of the primary butcher knife by nerve tissue that may contain the disease agent if the animal was infected. Also, avoid handling and consuming brain, spinal cord, lymph nodes, eyes, tonsils, and spleen when processing deer and elk from areas where CWD is known to be present.3032 Complete instructions on handling, testing, and disposing of deer and elk carcasses can be obtained from the Department of Natural Resources in the state where the deer or elk are to be harvested. Observations of deer or elk with the appearance of CWD should be reported to that agency.



Figure 5.28 Clinical signs and the unthrifty appearance of animals, rather than internal pathology, are indications of the potential that a deer or other cervid is infected with chronic wasting disease. Testing of appropriate tissue is required for a diagnosis.



http://www.nwhc.usgs.gov/publications/disease_emergence/Chapter5.pdf



Appendix C. Agents that require specific government approval for scientific investigations within the USA.a



Select agents, U.S. Department of Health and Human Services onlyb
High consequence pathogens and agents, U.S. Department of Agriculture onlyc
HIgh consequence livestock pathogens and toxins, overlap agents and toxinsd





(NO HUMAN TSE LISTED ???...tss) BSE agent 



http://www.nwhc.usgs.gov/publications/disease_emergence/AppendixC.pdf





HHS AND USDA SELECT AGENTS AND TOXINS 

7 CFR Part 331, 9 CFR Part 121, and 42 CFR Part 73 







http://www.cdc.gov/od/sap/docs/salist.pdf



Greetings list members,



confusious asks; 



WHY is it that BSE is listed as ;



Appendix C. Agents that require specific government approval for scientific investigations within the USA.a. ...



BUT, HUMAN TSE are NOT???



COULD you not do the same with a human TSE or other animal TSE ???



THE way the human tissue donor organ situation and the black market of that is set up, would not be too hard. ...



PRODUCTa) Product is 1.0 cc Regenaform® RT. SINGLE PATIENTUSE ONLY. Recall #
Z-0481-06;b) OPTEFORM Allografts of varying sizes. SINGLE PATIENTUSE ONLY.
Recall # Z-0482-06;c) Product is OPTEFORM Allograft Paste of varying
sizes.SINGLE PATIENT USE ONLY. Recall # Z-0483-06;d) OPTEFORM® RT Moldable
Allograft of varying sizes.SINGLE PATIENT USE ONLY. Recall # Z-0484-06;e)
Osteofil + RT Allograft Paste in varying sizes.SINGLE PATIENT USE ONLY.
Recall # Z-0485-06;f) Osteofil Allograft Paste (Bio) of varying sizes.SINGLE
PATIENT USE ONLY. Recall # Z-0486-06;g) Osteofil IC Syringeable of varying
sizes. SINGLEPATIENT USE ONLY. Recall # 0487-06;h) Osteofil ICM Moldable
Strip of varying sizes.SINGLE PATIENT USE ONLY. Recall # Z-0488-06;i)
Osteofil RT, ICM Allograft Paste of varying sizes.SINGLE PATIENT USE ONLY.
Recall # Z-0489-06;j) OSTEOFIL® DBM Paste of varying sizes. SINGLEPATIENT
USE ONLY. Recall # Z-0490-06;k) OsteoPack 3 FZ 22cc. SINGLE PATIENT USE
ONLY.Recall # Z-0491-06;l) Regenafil IC. SINGLE PATIENT USE ONLY.Recall #
Z-0492-06;m) REGENAFORM RT Allograft Paste, 1cc. SINGLEPATIENT USE ONLY.
Recall # Z-0493-06;n) Product is REGENAFORM® Allograft Moldable Blocks,of
varying sizes. SINGLE PATIENT USE ONLY.Recall # Z-0494-06;o) Product is RTI
Allograft Paste of varying sizes.SINGLE PATIENT USE ONLY. Recall #
Z-0495-06;p) Product is REGENAFIL® Allograft Paste, Syringe,0.5cc. SINGLE
PATIENT USE ONLY. Recall # 0496-06;q) Product is 1.0cc flowable paste from
donorapproved for distribution in Italy. SINGLEPATIENT USE ONLY. Recall #
Z-0497-06;r) Product is OPTEFIL Allograft Paste of varyingsizes. SINGLE
PATIENT USE ONLY. Recall# Z-0498-06;s) Product is OPTEFIL Allograft Paste,
Syringeof varying sizes. SINGLE PATIENT USE ONLY.Recall # Z-0499-06;t)
Product is OPTEFORM® Allograft Full Disc,5 x 90mm, 32cc, Frozen. SINGLE
PATIENT USEONLY, Recall # Z-0500-06;u) Product is 2.0 cc Opteform® RT.
SINGLEPATIENT USE ONLY. Recall # Z-0501-06CODE2879130 2879131 2879132
2879133 2879134 2879135 2879136 2879137 28791382879139 2879350 2879351
2879352 2879353 2879354 2879355 2879440 28794412879442 2879443 2879444
2879445 2879446 2879447 2879448 2879449 28794502879451 2879452 2879453
2879454 2879455 2879456 2879457 2879458



snip...literally 100s and 100s and 100s, much to many recalls to post here,
first few and last few lines posted here... TSS



2667981 2667983 2667984 2667985 26679872667988 2667989 2669552 2669553
2669554 2669556 2669559 2669633 26696362669639 2669640 2669965 2669967
2669968 2669969 2669981 2669983 2669985



RECALLING FIRM/MANUFACTURERRegeneration Technologies, Inc., Alachua, FL, by
letter on October 14, 2005.Firm initiated recall is ongoing.

REASON The tissue was collected from donors for whom there is

___no verifiableidentity or consent___.

The medical records and social histories of the donorscannot be ascertained.
The devices which incorporate these donor bonetissues undergo processing,
including sterilization, which has beenvalidated to inactivate and/or remove
all viral diseases for which humantissue donors are tested.



VOLUME OF PRODUCT IN COMMERCE 5,320 DISTRIBUTION



Nationwide and Internationally END OF ENFORCEMENT REPORT FOR FEBRUARY 15,
2006



###

http://www.fda.gov/bbs/topics/enforce/2006/ENF00939.html





FDA Public Health Notification: Update of Information about BioMedical Tissue Services
Posted: 3/2/2006 





FDA Public Health Notification*: 
Update of Information about BioMedical Tissue Services

March 2, 2006


FDA is issuing an update to its October 26, 2005, information paper on BioMedical Tissue Services (BTS) (http://www.fda.gov/bbs/topics/NEWS/2005/NEW01249.html) to strongly recommend that health care providers inform their patients who received tissue implants prepared from BTS donors that they may be at increased risk of communicable disease transmission and to offer them testing. As part of its ongoing investigation, FDA has become aware of additional information regarding the reliability of donor blood samples that is important for health care providers to consider. 

Background 

On October 26, 2005, FDA issued an information paper regarding its investigation of BTS (http://www.fda.gov/bbs/topics/NEWS/2005/NEW01249.html). FDA expressed concern that BTS had supplied tissue from donors that had not been subject to an adequate donor eligibility determination. FDA and CDC recommended that health care providers inform their patients of this potential risk and offer to provide access to appropriate infectious disease testing. 



snip...



full text ;



http://www.fda.gov/cber/safety/bts030206.htm



confusious is confused again in sunny Bacliff, Texas 



TSS

#################### https://lists.aegee.org/bse-l.html ####################


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## terry (Sep 13, 2002)

MAD COW i.e. all TSE 'FRIENDLY FIRE' GETTING SERIOUS (iCJD) 

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

CJD WATCH MESSAGE BOARD 
TSS 
Detection and Localization of PrPSc in the Skeletal Muscle 
Thu Mar 2, 2006 10:40 
70.110.86.250 


© 2006 American Society for Investigative Pathology 

Detection and Localization of PrPSc in the Skeletal Muscle of Patients with Variant, Iatrogenic, and Sporadic Forms of Creutzfeldt-Jakob Disease 
Alexander H. Peden, Diane L. Ritchie, Mark W. Head and James W. Ironside 
From the National Creutzfeldt-Jakob Disease Surveillance Unit and Division of Pathology, School of Molecular and Clinical Medicine, University of Edinburgh, Western General Hospital, Edinburgh, United Kingdom 


Variant Creutzfeldt-Jakob disease (vCJD) differs from other human prion diseases in that the pathogenic prion protein PrPSc can be detected to a greater extent at extraneuronal sites throughout the body, principally within lymphoid tissues. However, a recent study using a high-sensitivity Western blotting technique revealed low levels of PrPSc in skeletal muscle from a quarter of Swiss patients with sporadic CJD (sCJD). This posed the question of whether PrPSc in muscle could also be detected in vCJD, sCJD, and iatrogenic (iCJD) patients from other populations. Therefore, we have used the same high-sensitivity Western blotting technique, in combination with paraffin-embedded tissue blotting, to screen for PrPSc in muscle tissue specimens taken at autopsy from 49 CJD patients in the United Kingdom. These techniques identified muscle PrPSc in 8 of 17 vCJD, 7 of 26 sCJD, and 2 of 5 iCJD patients. Paraffin-embedded tissue blotting analysis showed PrPSc in skeletal muscle in localized anatomical structures that had the morphological and immunohistochemical characteristics of nerve fibers. The detection of PrPSc in muscle tissue from all forms of CJD indicates the possible presence of infectivity in these tissues, suggesting important implications for assessing the potential risk of iatrogenic spread via contaminated surgical instruments. 



http://ajp.amjpathol.org/cgi/content/abstract/168/3/927 




TSS 

#################### https://lists.aegee.org/bse-l.html #################### 



BSE ALSO; 


PrPSc distribution of a natural case of bovine spongiform encephalopathy 


Yoshifumi Iwamaru, Yuka Okubo, Tamako Ikeda, Hiroko Hayashi, Mori- kazu Imamura, Takashi Yokoyama and Morikazu Shinagawa Priori Disease Research Center, National Institute of Animal Health, 3-1-5 Kannondai, Tsukuba 305-0856 Japan [email protected] 


Abstract 


Bovine spongiform encephalopathy (BSE) is a disease of cattle that causes progressive neurodegeneration of the central nervous system. Infectivity of BSE agent is accompanied with an abnormal isoform of prion protein (PrPSc). The specified risk materials (SRM) are tissues potentially carrying BSE infectivity. The following tissues are designated as SRM in Japan: the skull including the brain and eyes but excluding the glossa and the masse- ter muscle, the vertebral column excluding the vertebrae of the tail, spinal cord, distal illeum. For a risk management step, the use of SRM in both animal feed or human food has been prohibited. However, detailed PrPSc distribution remains obscure in BSE cattle and it has caused controversies 
about definitions of SRM. Therefore we have examined PrPSc distribution in a BSE cattle by Western blotting to reassess definitions of SRM. The 11th BSE case in Japan was detected in fallen stock surveillance. The carcass was stocked in the refrigerator. For the detection of PrPSc, 200 mg of tissue samples were homogenized. Following collagenase treatment, samples were digested with proteinase K. After digestion, PrPSc was precipitated by sodium phosphotungstate (PTA). The pellets were subjected to Western blotting using the standard procedure. Anti-prion protein monoclonal antibody (mAb) T2 conjugated horseradish peroxidase was used for the detection of PrPSc. PrPSc was detected in brain, spinal cord, dorsal root ganglia, trigeminal ganglia, sublingual ganglion, retina. In addition, PrPSc was also detected in the peripheral nerves (sciatic nerve, tibial nerve, vagus nerve). Our results suggest that the currently accepted definitions of SRM in 9/13/2005 


179 
Page 10 of 17 



BSE cattle may need to be reexamined. 


T. Kitamoto (Ed.) 
PRIONS 
Food and Drug Safety 

================ 

ALSO from the International Symposium of Prion Diseases held in Sendai, October 31, to November 2, 2004; Bovine spongiform encephalopathy (BSE) in Japan 

snip... 


"Furthermore, current studies into transmission of cases of BSE that are atypical or that develop in young cattle are expected to amplify the BSE prion" NO. Date conf. Farm Birth place and Date Age at diagnosis 8. 2003.10.6. Fukushima Tochigi 2001.10.13. 23 9. 2003.11.4. Hiroshima Hyogo 2002.1.13. 21 Test results # 8b, 9c cows Elisa Positive, WB Positive, IHC negative, histopathology negative b = atypical BSE case c = case of BSE in a young animal b,c, No PrPSc on IHC, and no spongiform change on histology International Symposium of Prion Diseases held in Sendai, October 31, to November 2, 2004. Tetsuyuki Kitamoto Professor and Chairman Department of Prion Research Tohoku University School of Medicine 2-1 SeiryoAoba-ku, Sendai 980-8575, JAPAN TEL +81-22-717-8147 FAX +81-22-717-8148 e-mail; [email protected] Symposium Secretariat Kyomi Sasaki TEL +81-22-717-8233 FAX +81-22-717-7656 e-mail: [email protected] ================================= 9/13/2005 
-------------------------------------------------------------------------------- 
-------------------------------------------------------------------------------- 
Page 11 of 17 From: TSS () Subject: Atypical Proteinase K-Resistant Prion Protein (PrPres) observed in an Apparently Healthy 23-Month-Old Holstein Steer Date: August 26, 2005 at 10:24 am PST Atypical Proteinase K-Resistant Prion Protein (PrPres) observed in an Apparently Healthy 23-Month-Old Holstein Steer Jpn. J. Infect. Dis., 56, 221-222, 2003 Laboratory and Epidemiology Communications Atypical Proteinase K-Resistant Prion Protein (PrPres) Observed in an Apparently Healthy 23-Month-Old Holstein Steer Yoshio Yamakawa*, KenÕichi Hagiwara, Kyoko Nohtomi, Yuko Nakamura, Masahiro Nishizima ,Yoshimi Higuchi1, Yuko Sato1, Tetsutaro Sata1 and the Expert Committee for BSE Diagnosis, Ministry of Health, Labour and Welfare of Japan2 Department of Biochemistry & Cell Biology and 1Department of Pathology, National Institute of Infectious Diseases, Tokyo 162-8640 and 2Miistry of Health, Labour and Welfare, Tokyo 100-8916 Communicated by Tetsutaro Sata (Accepted December 2, 2003) *Corresponding author: Mailing address: Department of Biochemistry and Cell Biology, National Institute of Infectious Diseases, Toyama 1-23-1, Shinjuku-ku, Tokyo 1628640, 
Japan. Tel: +81-3-5285-1111, Fax: +81-3-5285-1157, E-mail: [email protected] 


Since October 18, 2001, 'bovine spongiform encephalopathy (BSE) examination for all cattle slaughtered at abattoirs in the country' has been mandated in Japan by the Ministry of Health, Labour and Welfare (MHLW). 'Plateria' ELISA-kit (Bio-Rad Laboratories, Hercules, Calif., USA) is routinely used at abattoirs for detecting proteinase K (PK)-resistant prion protein (PrPSc) in the obex region. Samples positive according to the ELISA screening are further subjected to Western blot (WB) and histologic and immunohistochemical examination (IHC) at the National Institute of Infectious Diseases (NIID) or Obihiro University. If PrPSc is detected either by WB or by IHC, the cattle are diagnosed as BSE. The diagnosis is approved by the Expert Committee for BSE Diagnosis, MHLW. From October 18, 2001 to September 30, 2003, approximately 2.5 million cattle were screened at abattoirs. A hundred and ten specimens positive according to ELISA were subjected to WB/IHC. Seven showed positive by both WB and IHC, all exhibiting the typical electrophoretic profile of a high content of the di-glycosylated molecular form of PrPSc (1-3) and the distinctive granular deposition of PrPSc in neuronal cells and neuropil of the dorsal nucleus of vagus. An ELISA-positive specimen from a 23 month-old Holstein steer slaughtered on September 29, 2003, in Ibaraki Prefecture (Ibaraki case) was sent to the NIID for confirmation. The animal was reportedly healthy before slaughter. The OD titer in ELISA was slightly higher than the 'cut-off' level given by the manufacturer. The histology showed no spongiform changes and IHC revealed no signal of PrPSc accumulation typical for BSE. However, WB analysis of the homogenate that was prepared from the obex region and used for ELISA revealed a small amount of PrPSc with an electrophoretic profile different from that of typical BSE-associated PrPSc (1-3). The characteristics were (i) low content of the di-glycosylated molecular form of PrPSc, (ii) a faster migration of the non-glycosylated form of PrPSc on SDS-PAGE, and (iii) less resistance against PK digestion as compared with an authentic PrPSc specimen derived from an 83-month-old Holstein (Wakayama case) (Fig. 1). Table 1 summarizes the relative amounts of three distinctive glycoforms (di-, mono, non-glycosylated) of PrPSc calculated by densitometric analysis of the blot shown in Fig. 1. As 2.5 mg wet weight obex-equivalent homogenate of the Ibaraki case (Fig. 1, lane 4) gave slightly stronger band intensities of PrPSc than an 8 mg wet weight obex-equivqlent homogenate of a typical BSE-affected Wakayama case (Fig. 1, lane 2), the amount of PrPSc accumulated in the Ibaraki case was calculated to be 1/500 - 1/1000 of the Wakayama case. In the Ibaraki case, the PrPSc bands were not detectable in the homogenates of the proximal surrounding region of the obex. These findings were consistent with the low OD value in ELISA, i.e., 0.2 -0.3 for the Ibaraki case versus over 3.0 for the Wakayama case. The DNA sequence of the PrP coding region of the Ibaraki case was the same as that appearing in the database (GenBank accession number: AJ298878). More recently, we encountered another case that resembled the Ibaraki case. It was a 21-monthold 
Holstein steer from Hiroshima Prefecture. WB showed typical BSE-specific PrPSc deposition though IHC did not detect positive signals of PrPSc (data not shown). Though the clinical onset of BSE is usually at around 5 years of age or later, a 20-month-old case showing the clinical signs has been reported (4). Variant forms of BSE similar to our cases, i.e., with atypical histopathological and/or biochemical phenotype, have been recently reported in Italy (5) and in France (6). Such variant BSE was not associated with mutations in the prion protein (PrP) coding region as in our case (5,6). The Ministry of Agriculture, Forestry and Fisheries of Japan (MAFF) announced a ban of feeding ruminants with meat bone meal (MBM) on September 18, 2001, and a complete ban was made on October 15 of the same year. According to the recent MAFF report, the previous seven cases of BSE in Japan were cattle born in 1995 - 1996 and possibly fed with cross-contaminated feed. However, the two cattle in this report were born after the complete ban. Whether contaminated MBM was implicated in the present cases remains to be investigated. 



REFERENCES Collinge, J., Sidle, K. C. L., Meads, J., Ironside, J. and Hill, A. F. (1996): Molecular analysis of prion strain variation and the aetiology of 'new variant' CJD. Nature, 383, 685690. 
Bruce, M. E., Will, R. G., Ironside, J. W., McConnell, I., Drummond, D., Suttie, A., McCardle, L., Chree, A., Hope, J., Birkett, C., Cousens, S., Fraser, H. and Bostock, C. J. 
(1997): Transmissions to mice indicate that 'new variant' CJD is caused by the BSE agent. Nature, 389, 498-501. 
Hill, A. F., Desbruslais, M., Joiner, S., Sidle, K. C. L., Gowland, I. and Collinge, J. (1997): The same prion strain causes vCJD and BSE. Nature, 389, 448-450. 
Matravers, W., Bridgeman, J. and Smith, M.-F. (ed.)(2000): The BSE Inquiry. p. 37. vol. 16. The Stationery Office Ltd., Norwich, UK. 
Casalone, C., Zanusso, G., Acutis, P. L., Crescio, M. I., Corona, C., Ferrari, S., Capobianco, R., Tagliavini, F., Monaco, S. and Caramelli, M. (2003): Identification of a novel 
molecular and neuropathological BSE phenotype in Italy. International Conference on Prion Disease: from basic research to intervention concepts. Gasreig, Munhen, 
October 8-10. 
Bicaba, A. G., Laplanche, J. L., Ryder, S. and Baron, T. (2003): A molecular variant of bovine spongiform encephalopatie. International Conference on Prion Disease: from 
basic research to intervention concepts. Gasreig, Munhen, October 8-10. 
Asante, E. A., Linehan, J. M., Desbruslais, M., Joiner, S., Gowland, I., Wood, A. L., Welch, J., Hill, A. F., Lloyd, S. E., Wadsworth, J. D. F. and Collinge, J. (2002). BSE 
prions propagate as either variant CJD-like or sporadic CJD-like prion strains in transgenic mice expressing human prion protein. EMBO J., 21, 6358-6366. 
9/13/2005 
Page 12 of 17 SEE SLIDES IN PDF FILE; http://www.nih.go.jp/JJID/56/221.pdf 


http://www.fsis.usda.gov/OPPDE/Comments/03-025IFA/03-025IFA-2.pdf 



AND CWD; 


Prions in Skeletal Muscles of Deer with Chronic Wasting Disease Rachel C. Angers,1* Shawn R. Browning,1* Tanya S. Seward,2 Christina J. Sigurdson,4 Michael W. Miller,5 Edward A. Hoover,4 Glenn C. Telling1,2,3§ 1Department of Microbiology, Immunology and Molecular Genetics, 2Sanders Brown Center on Aging, 3Department of Neurology, University of Kentucky, Lexington, KY 40536, USA. 4Department of Microbiology, Immunology and Pathology, Colorado State University, Fort Collins, CO 80523, USA. 5Colorado Division of Wildlife, Wildlife Research Center, Fort Collins, CO 80526, USA. *These authors contributed equally to this work. Present address: Department of Infectology, Scripps Research Institute, 5353 Parkside Drive, RF-2, Jupiter, Florida, 33458, USA. Present address: Institute of Neuropathology, University of Zurich, Schmelzbergstrasse 12, 8091 Zurich, Switzerland. §To whom correspondence should be addressed: E-mail: [email protected] Prions are transmissible proteinaceous agents of mammals that cause fatal neurodegenerative diseases of the central nervous system (CNS). The presence of infectivity in skeletal muscle of experimentally infected mice raised the possibility that dietary exposure to prions might occur through meat consumption (1). Chronic wasting disease (CWD), an enigmatic and contagious prion disease of North American cervids, is of particular concern. The emergence of CWD in an increasingly wide geographic area and the interspecies transmission of bovine spongiform encephalopathy (BSE) to humans as variant Creutzfeldt Jakob disease (vCJD) have raised concerns about zoonotic transmission of CWD. To test whether skeletal muscle of diseased cervids.........SNIP....END 

===============================

1: J Neurol Neurosurg Psychiatry 1994 Jun;57(6):757-8

Transmission of Creutzfeldt-Jakob disease to a chimpanzee by electrodes contaminated during neurosurgery.

Gibbs CJ Jr, Asher DM, Kobrine A, Amyx HL, Sulima MP, Gajdusek DC.

Laboratory of Central Nervous System Studies, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892.

Stereotactic multicontact electrodes used to probe the cerebral cortex of a middle aged woman with progressive dementia were previously implicated in the accidental transmission of Creutzfeldt-Jakob disease (CJD) to two younger patients. The diagnoses of CJD have been confirmed for all three cases. More than two years after their last use in humans, after three cleanings and repeated sterilisation in ethanol and formaldehyde vapour, the electrodes were implanted in the cortex of a chimpanzee. Eighteen months later the animal became ill with CJD. This finding serves to re-emphasise the potential danger posed by reuse of instruments contaminated with the agents of spongiform encephalopathies, even after scrupulous attempts to clean them.

PMID: 8006664 [PubMed - indexed for MEDLINE]
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8006664&dopt=Abstract

TSS


TSS


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