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From: TSS ()
Subject: Creutzfeldt-Jakob disease (CJD) update report iatrogenic exposure to CJD
Date: May 11, 2006 at 9:36 am PST


Creutzfeldt-Jakob disease (CJD) update report

This six-monthly report provides an update on reports of incidents of potential iatrogenic (healthcare-acquired) exposure to Creutzfelt-Jakob disease (CJD) via surgery, and on the National Anonymous Tonsil Archive. Numbers of CJD case reports can be found on the national CJD Surveillance Unit (NCJDSU) [1]. The latest quarterly analysis of vCJD reports (onsets and deaths) is also available from the NCJDSU website [2].

Reports of incidents of potential iatrogenic exposure to CJD via surgery: September 2004 to August 2005

During the year September 2004 to August 2005, 62 incidents of potential exposure to CJD via surgical instruments were reported to the CJD Incidents Panel. Surgical incidents occur when instruments considered potentially contaminated with the CJD agent during use on an index patient have been subsequently re-used on other patients. The patient whose surgery results in potential contamination of instruments is referred to as the index patient. Table 1 shows the number of CJD surgical incidents reported to the CJD Incidents Panel during the five years August 2000 to August 2005 by the diagnosis of the index patient.

Table 1 CJD Surgical Incidents (n=235) reported to the CJD Incidents Panel, by diagnosis of index patient: August 2000 and August 2005


Final diagnosis of index patient Year 1 to 4 Year 5 Total
28/08/00-31/08/2004 01/09/04-31/08/2005 Aug 2000-Aug-05
Sporadic CJD (possible,
probable or definite) 81 16 97
Variant CJD(possible,
probable, or definite) 45 2 47
Other types of CJD, or 'at risk'
of CJD, or CJD type unclear 33 42 75
Not CJD 14 2 16
Total 173 62 235

Investigation of surgical incidents occasionally resulted in advice to remove surgical instruments from use on other patients (to quarantine, destroy, or donate for research). Hospitals are asked to consider sending any instruments to be permanently removed from use to the Surgical Instrument Store (held by the Health Protection Agency [HPA], Porton Down) to be used for research purposes.

In year five, (ie, from 1 September 2004 to 31 August 2005), the Panel advised that instruments should be permanently removed from use on other patients following use on the index patient in seven incidents. Advice to contact and inform patients of their potential exposure to CJD via surgical instruments was given in one incident. Information about the CJD Incidents Panel can be found on the HPA website [3].

The National Anonymous Tonsil Archive
The National Anonymous Tonsil Archive (NATA) is a national unlinked anonymous survey of tonsil tissue that will be used to undertake studies on the prevalence of abnormal prion protein, the agent believed to be responsible for infection with variant Creutzfeldt-Jakob Disease (vCJD) [4]. NATA began it's activities at the end of 2003 and aims to collect 100,000 pairs of tonsils. Tonsils are being collected from people of all ages during routine tonsillectomies. The archive only includes tissue which is not required for patient care, and would normally be discarded. Patients are given an opportunity to object to their tissues being used in the archive.

By the end of April 2006, 25,209 tonsil pairs had been collected. In addition, 1087 collection forms were completed without accompanying tonsil tissue (730 due to patient objection and 357 due to clinical pathology having been requested on the specimen as part of the patient's care). Figure 1 shows the number of tonsil pairs received per month between January 2004 and April 2006.

Figure 1 Number of tonsil pairs collected for NATA monthly: January 2004 to April 2006

By April 2006, 76 of the 100 NHS hospital trusts that perform more than 200 tonsillectomies per year in England were regularly sending tonsil pairs to NATA. Recruitment of hospitals continues, with the expectation that the target recruitment rate of 500 tonsil pairs per week will be met. Approximately 50,000 tonsillectomies are currently performed annually in England.

The project has recently started in Scotland where just over 5000 tonsillectomies are performed each year. There are 14 hospitals in Scotland that carry out more than 200 tonsillectomies per year and these hospitals are being visited by a team of liaison officers so that procedures for the collection of tonsil tissue after tonsillectomies are successfully adopted. By April 2006, six of the hospitals in Scotland had begun sending tonsil tissue to the archive.

Figure 2 NHS hospital trusts currently sending tonsils to NATA

References

1. The National Creutzfeldt-Jakob Disease Surveillance Unit, The University of Edinburgh. CJD statistics. CJD figures. Edinburgh: NCJDSU, 3 May 2005. Available at
.

2.The National Creutzfeldt-Jakob Disease Surveillance Unit, The University of Edinburgh. Incidence of variant Creutzfeldt-Jakob Disease Onsets and Deaths in the UK January 1994 – March 2005. Edinburgh: NCJDSU, 14 April 2005. Available at .

3. Health Protection Agency [online]. CJD Incidents Panel. London: HPA. Available at
.

4. HPA. The National Anonymous Tonsil Archive: a resource for Creutzfeldt-Jakob disease studies. Commun Dis Rep CDR Wkly [serial online] 30 October 2003 [cited 11 May 2005]; 13(44): News. Available at: .

http://www.hpa.org.uk/cdr/archives/2006/cdr1906.pdf

SEAC Position statement vCJD and Endodontic dentistry
Issue

http://www.seac.gov.uk/statements/statement0506.htm

The CJD Incidents Panel had been provided with the SEAC

advice from SEAC 91 on the assessment of potential risks

from medical implants containing bovine material.

CONCENTRATION OF vCJD INFECTIVITY IN BLOOD

COMPONENTS

The UK Blood Service and DH asked SEAC to consider TSE

infectivity in whole blood and blood components and other issues

relating to assessment of the risks of vCJD transmission via blood

transfusion. The discussion was held in a reserved business

session to allow consideration of unpublished research. The

committee agreed to produce a statement of its conclusions.


http://www.seac.gov.uk/summaries/seac92_summary.pdf

8 May 2006 - Final minutes of SEAC 91 meeting

http://www.seac.gov.uk/minutes/final91.pdf


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 gan@affrc.go.jp


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; kitamoto@mail.tains.tohoku.ac.jp Symposium Secretariat Kyomi Sasaki TEL +81-22-717-8233 FAX +81-22-717-7656 e-mail: kvomi-sasaki@mail.tains.tohoku.ac.ip ================================= 9/13/2005
--------------------------------------------------------------------------------
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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*, KenŐichi 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: yamakawa@nih.go.jp


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: gtell2@uky.edu 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

TSS





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