Showing posts with label USA. Show all posts
Showing posts with label USA. Show all posts

Thursday, December 23, 2010

Molecular Typing of Protease-Resistant Prion Protein in Transmissible Spongiform Encephalopathies of Small Ruminants, France, 2002–2009

Volume 17, Number 1–January 2011

Research

Molecular Typing of Protease-Resistant Prion Protein in Transmissible Spongiform Encephalopathies of Small Ruminants, France, 2002–2009

Johann Vulin, Anne-Gaëlle Biacabe, Géraldine Cazeau, Didier Calavas, and Thierry Baron Author affiliation: Agence Nationale de Sécurité Sanitaire, Lyon, France

Suggested citation for this article

Abstract The agent that causes bovine spongiform encephalopathy (BSE) may be infecting small ruminants, which could have serious implications for human health. To distinguish BSE from scrapie and to examine the molecular characteristics of the protease-resistant prion protein (PrPres), we used a specifically designed Western blot method to test isolates from 648 sheep and 53 goats. During 2002–2009, classical non-Nor98 transmissible spongiform encephalopathy had been confirmed among ˜1.7 million small ruminants in France. Five sheep and 2 goats that showed a PrPres pattern consistent with BSE, or with the CH1641 experimental scrapie source, were identified. Later, bioassays confirmed infection by the BSE agent in 1 of the 2 goats. Western blot testing of the 6 other isolates showed an additional C-terminally cleaved PrPres product, with an unglycosylated band at ˜14 kDa, similar to that found in the CH1641 experimental scrapie isolate and different from the BSE isolate.

snip...

Discussion We investigated the PrPres molecular features of one of the largest series of natural TSE isolates from sheep and goats analyzed so far in Europe. Approximately 1.7 million small ruminants were subjected to a rapid test; among these, 1,153 sheep and 78 goats originating from 992 flocks were confirmed as TSE-positive on the basis of identification of PrPres in the brain stem. Another large study using 1,247 sheep originating from 450 flocks in Great Britain has been reported (24). Similar studies have been conducted in other European countries such as Germany (34), the Netherlands (14), and Italy (23), but fewer TSE-positive animals were reported. In our series, animals with classical cases represented 53% of the TSE-affected animals.

The molecular features of most of these isolates (99%) were comparable to those previously described for most scrapie cases, in studies in Europe or France (21). In all of these cases, PrPres from sheep and goats showed clearly distinct features from BSE, based on the identification of a higher molecular mass of unglycosylated PrPres, associated with strong labeling by the P4 antibody that recognizes the N terminal end of the protein. However, our observation of large individual variations in this PrPres molecular mass implies that a possible relationship with the biologic diversity of TSE agents, which has been described after transmission of scrapie to inbred wild-type mice (35), would be questionable. Only a few animals (5 sheep and 2 goats) in this large series of TSE-affected animals showed molecular characteristics that, in comparison with the usual features of scrapie, could be consistent with the known BSE signature in small ruminants. These samples represented all the suspected isolates that were identified by official surveillance in France during 2002–2009.

An essential molecular criterion defined from the observation of PrPres BSE compared with scrapie was the low molecular mass of the unglycosylated band in PrPres BSE, associated with a decreased PrPres signal lower with an N terminal antibody than with a core antibody (13,22,36). After identification of these molecular features in a few small ruminants, only 1 (CH636) of the 2 cases here described in goats, identified as TSE positive in 2002, has been shown to be infected by the BSE agent after bioassays in mice (37). Another goat in the United Kingdom identified by an immunohistochemical discriminatory method as TSE-positive in 1990 showed characteristics that were indistinguishable from BSE (18). These results clearly indicate that in a situation characterized by a decrease in the number of cases in cattle in all countries in Europe, the possibility of finding BSE in small ruminants is now remote.

The other unusual isolates showed molecular characteristics that were partly similar, not only to BSE in small ruminants with a low molecular mass of PrPres and faint labeling with P4 antibody, but also to the CH1641 experimental scrapie isolate. However, detailed immunohistochemical investigations of CH1641 showed subtle differences in the cleavage site of the protein compared with BSE in sheep (38). As previously described, after transmission in ovine transgenic mice (17), the slightly lower PrPres molecular mass in CH1641-like isolates, as recognized in the CH1641 experimental isolate (13) was confirmed by Western blot, at least in sheep (Figure 2, panel B). However, these differences in molecular mass are more easily identified on the diglycosylated band. Compared with BSE in small ruminants, lower proportions of this diglycosylated band were found in sheep, whereas the 08-357 goat sample showed very high levels of this diglycosylated band, which would be consistent with BSE. Experimental transmissions of BSE in sheep have shown that, to a certain extent, the PrPres molecular features could be influenced by different factors, such as serial passages in sheep (39) or sheep genotypes (36), although slight variability did not compromise the discrimination with scrapie. Furthermore, all these CH1641-like natural isolates in sheep and goats clearly differed from BSE by the presence of an additional, C-terminally cleaved, PrPres product specifically recognized by a C-terminal antibody (SAF84), as previously described for the CH1641 experimental scrapie isolate (17). Baron et al. described bioassays of 3 of 20 CH1641-like sheep isolates (17), which are also being conducted for the other isolates.

These 6 CH1641-like isolates were identified among 1,153 sheep and 78 goats with confirmed TSE, and the goat case represents, to our knowledge, a spreading of the known species range for natural CH1641 infection. At least in sheep, for which 4.34 cases per million sheep tested were identified in this study, the frequency of CH1641-like scrapie was notably higher compared with other rare TSEs in ruminants such as atypical BSEs, which showed a frequency of 0.76 per million cattle tested during 2001–2007 (40). Thus, large-scale testing of animals would be required to identify these rare TSE isolates. Similar isolates were only identified in sheep in the other large series reported from 450 flocks in Great Britain (2 cases in 1 flock) (23) and in a previous study of 214 TSE-infected sheep in France (2 cases in 1 flock) (27). However, an underestimation of the frequency of such cases cannot be fully excluded. PrPres features are assessed by analyzing a single homogenate prepared from a brain fragment from the animal. Stack et al. described a case in sheep that appeared as CH1641-like after repeated Western blot analysis of a brain stem sample, whereas previous analysis of the caudal medulla at the time of submission had shown the usual scrapie profile (24). Immunohistochemical testing of 2 CH1641-like cases in sheep showed, that unlike BSE, PrPd could be clearly identified by using P4 antibody in some of the brain stem nuclei and in lymphoid tissues (27). Finally, on the basis of identification of low levels of C-terminal PrPres product in ovine transgenic mice infected with usual scrapie isolates, we hypothesized that a CH1641-like component might be present as a minor component in these scrapie cases that showed usual molecular features (17). All these data raise the question of the existence of possible mixtures of TSE agents in these particular CH1641-like isolates.


please see full text ;


http://www.cdc.gov/eid/content/17/1/55.htm



Sunday, December 12, 2010

EFSA reviews BSE/TSE infectivity in small ruminant tissues News Story 2 December 2010


snip...


One of these isolates (TR316211) behaved like the CH1641 isolate, with PrPres features in mice similar to those in the sheep brain. From two other isolates (O100 and O104), two distinct PrPres phenotypes were identified in mouse brains, with either high (h-type) or low (l-type) apparent molecular masses of unglycosylated PrPres, the latter being similar to that observed with CH1641, TR316211, or BSE. Both phenotypes could be found in variable proportions in the brains of the individual mice. In contrast with BSE, l-type PrPres from "CH1641-like" isolates showed lower levels of diglycosylated PrPres. From one of these cases (O104), a second passage in mice was performed for two mice with distinct PrPres profiles. This showed a partial selection of the l-type phenotype in mice infected with a mouse brain with predominant l-type PrPres, and it was accompanied by a significant increase in the proportions of the diglycosylated band. These results are discussed in relation to the diversity of scrapie and BSE strains.

http://jvi.asm.org/cgi/content/full/81/13/7230?view=long&pmid=17442721


In the US, scrapie is reported primarily in sheep homozygous for 136A/171Q (AAQQ) and the disease phenotype is similar to that seen with experimental strain CH1641.

http://www.ars.usda.gov/research/publications/publications.htm?seq_no_115=182469


4.2.9 A further hypothesis to explain the occurrence of BSE is the emergence or selection of a strain or strains of the scrapie agent pathogenic for cattle. Mutations of the scrapie agent. which can occur after a single passage in mice. have been well documented (9). This phenomenon cannot be dismissed for BSE. but given the form of the epidemic and the geographically widespread occurrence of BSE, such a hypothesis" would require the emergence of a mutant scrapie strain simultaneously in a large . number of sheep flocks, or cattle. throughout the country. Also. if it resulted "from a localised chance transmission of the scrapie strain from sheep to cattle giving rise , . to a mutant. a different pattern of disease would have been expected: its range would '. have increased with time. Thus the evidence from Britain is against the disease being due to a new strain of the agent, but we note that in the United States from 1984 to 1988 outbreaks of scrapie in sheep flocks are reported to have Increased markedly. now being nearly 3 times as high as during any previous period (18).

http://collections.europarchive.org/tna/20080102132706/http://www.bseinquiry.gov.uk/files/ib/ibd1/tab02.pdf


If the scrapie agent is generated from ovine DNA and thence causes disease in other species, then perhaps, bearing in mind the possible role of scrapie in CJD of humans (Davinpour et al, 1985), scrapie and not BSE should be the notifiable disease. ...

http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1988/06/08004001.pdf


http://scrapie-usa.blogspot.com/2007/12/scrapie-hb-parry-seriously-yb886841.html


EVIDENCE OF SCRAPIE IN SHEEP AS A RESULT OF FOOD BORNE EXPOSURE

This is provided by the statistically significant increase in the incidence of sheep scrape from 1985, as determined from analyses of the submissions made to VI Centres, and from individual case and flock incident studies. ........

http://web.archive.org/web/20010305222246/www.bseinquiry.gov.uk/files/yb/1994/02/07002001.pdf


RISK OF BSE TO SHEEP VIA FEED

http://collections.europarchive.org/tna/20090114022605/http://www.bseinquiry.gov.uk/files/sc/seac31/tab01.pdf


Marion Simmons communicated surprising evidence for oral transmissibility of Nor98/atypical scrapie in neonatal sheep and although bioassay is ongoing, infectivity of the distal ileum of 12 and 24 month infected sheep is positive in Tg338 mice.

http://www.goatbse.eu/site/index.php?option=com_content&view=article&id=94:minutes-workshop-2010&catid=9:popular&Itemid=22


SUMMARY REPORTS OF MAFF BSE TRANSMISSION STUDIES AT THE CVL ;

http://collections.europarchive.org/tna/20090114023010/http://www.bseinquiry.gov.uk/files/sc/seac18/tab02b.pdf


THE RISK TO HUMANS FROM SHEEP;

http://collections.europarchive.org/tna/20090114022915/http://www.bseinquiry.gov.uk/files/sc/seac24/tab03.pdf


EXPERIMENTAL TRANSMISSION OF BSE TO SHEEP

http://collections.europarchive.org/tna/20090114023211/http://www.bseinquiry.gov.uk/files/sc/seac25/tab05.pdf


SHEEP AND BSE

PERSONAL AND CONFIDENTIAL

SHEEP AND BSE

A. The experimental transmission of BSE to sheep.

Studies have shown that the ''negative'' line NPU flock of Cheviots can be experimentally infected with BSE by intracerebral (ic) or oral challenge (the latter being equivalent to 0.5 gram of a pool of four cow brains from animals confirmed to have BSE).

http://collections.europarchive.org/tna/20090506010048/http://www.bseinquiry.gov.uk/files/sc/seac33/tab02.pdf


RB264

BSE - TRANSMISSION STUDIES

http://collections.europarchive.org/tna/20090113230127/http://www.bseinquiry.gov.uk/files/sc/Seac06/tab06.pdf


1: J Infect Dis 1980 Aug;142(2):205-8

Oral transmission of kuru, Creutzfeldt-Jakob disease, and scrapie to nonhuman primates.

Gibbs CJ Jr, Amyx HL, Bacote A, Masters CL, Gajdusek DC.

Kuru and Creutzfeldt-Jakob disease of humans and scrapie disease of sheep and goats were transmitted to squirrel monkeys (Saimiri sciureus) that were exposed to the infectious agents only by their nonforced consumption of known infectious tissues. The asymptomatic incubation period in the one monkey exposed to the virus of kuru was 36 months; that in the two monkeys exposed to the virus of Creutzfeldt-Jakob disease was 23 and 27 months, respectively; and that in the two monkeys exposed to the virus of scrapie was 25 and 32 months, respectively. Careful physical examination of the buccal cavities of all of the monkeys failed to reveal signs or oral lesions. One additional monkey similarly exposed to kuru has remained asymptomatic during the 39 months that it has been under observation.

snip...

The successful transmission of kuru, Creutzfeldt-Jakob disease, and scrapie by natural feeding to squirrel monkeys that we have reported provides further grounds for concern that scrapie-infected meat may occasionally give rise in humans to Creutzfeldt-Jakob disease.

PMID: 6997404

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6997404&dopt=Abstract


12/10/76 AGRICULTURAL RESEARCH COUNCIL REPORT OF THE ADVISORY COMMITTE ON SCRAPIE Office Note CHAIRMAN: PROFESSOR PETER WILDY

snip...

A The Present Position with respect to Scrapie A] The Problem Scrapie is a natural disease of sheep and goats. It is a slow and inexorably progressive degenerative disorder of the nervous system and it ia fatal. It is enzootic in the United Kingdom but not in all countries. The field problem has been reviewed by a MAFF working group (ARC 35/77). It is difficult to assess the incidence in Britain for a variety of reasons but the disease causes serious financial loss; it is estimated that it cost Swaledale breeders alone $l.7 M during the five years 1971-1975. A further inestimable loss arises from the closure of certain export markets, in particular those of the United States, to British sheep. It is clear that scrapie in sheep is important commercially and for that reason alone effective measures to control it should be devised as quickly as possible. Recently the question has again been brought up as to whether scrapie is transmissible to man. This has followed reports that the disease has been transmitted to primates.

One particularly lurid speculation (Gajdusek 1977) conjectures that the agents of scrapie, kuru, Creutzfeldt-Jakob disease and transmissible encephalopathy of mink are varieties of a single "virus". The U.S. Department of Agriculture concluded that it could "no longer justify or permit scrapie-blood line and scrapie-exposed sheep and goats to be processed for human or animal food at slaughter or rendering plants" (ARC 84/77)" The problem is emphasised by the finding that some strains of scrapie produce lesions identical to the once which characterise the human dementias" Whether true or not. the hypothesis that these agents might be transmissible to man raises two considerations. First, the safety of laboratory personnel requires prompt attention. Second, action such as the "scorched meat" policy of USDA makes the solution of the acrapie problem urgent if the sheep industry is not to suffer grievously.

snip...

76/10.12/4.6

http://web.archive.org/web/20010305223125/www.bseinquiry.gov.uk/files/yb/1976/10/12004001.pdf


Nature. 1972 Mar 10;236(5341):73-4.

Transmission of scrapie to the cynomolgus monkey (Macaca fascicularis).

Gibbs CJ Jr, Gajdusek DC. Nature 236, 73 - 74 (10 March 1972); doi:10.1038/236073a0

Transmission of Scrapie to the Cynomolgus Monkey (Macaca fascicularis)

C. J. GIBBS jun. & D. C. GAJDUSEK National Institute of Neurological Diseases and Stroke, National Institutes of Health, Bethesda, Maryland

SCRAPIE has been transmitted to the cynomolgus, or crab-eating, monkey (Macaca fascicularis) with an incubation period of more than 5 yr from the time of intracerebral inoculation of scrapie-infected mouse brain. The animal developed a chronic central nervous system degeneration, with ataxia, tremor and myoclonus with associated severe scrapie-like pathology of intensive astroglial hypertrophy and proliferation, neuronal vacuolation and status spongiosus of grey matter. The strain of scrapie virus used was the eighth passage in Swiss mice (NIH) of a Compton strain of scrapie obtained as ninth intracerebral passage of the agent in goat brain, from Dr R. L. Chandler (ARC, Compton, Berkshire).

http://www.nature.com/nature/journal/v236/n5341/abs/236073a0.html


Epidemiology of Scrapie in the United States 1977

http://web.archive.org/web/20030513212324/http://www.bseinquiry.gov.uk/files/mb/m08b/tab64.pdf


Sunday, April 18, 2010

SCRAPIE AND ATYPICAL SCRAPIE TRANSMISSION STUDIES A REVIEW 2010

http://scrapie-usa.blogspot.com/2010/04/scrapie-and-atypical-scrapie.html


One of these isolates (TR316211) behaved like the CH1641 isolate, with PrPres features in mice similar to those in the sheep brain. From two other isolates (O100 and O104), two distinct PrPres phenotypes were identified in mouse brains, with either high (h-type) or low (l-type) apparent molecular masses of unglycosylated PrPres, the latter being similar to that observed with CH1641, TR316211, or BSE. Both phenotypes could be found in variable proportions in the brains of the individual mice. In contrast with BSE, l-type PrPres from "CH1641-like" isolates showed lower levels of diglycosylated PrPres. From one of these cases (O104), a second passage in mice was performed for two mice with distinct PrPres profiles. This showed a partial selection of the l-type phenotype in mice infected with a mouse brain with predominant l-type PrPres, and it was accompanied by a significant increase in the proportions of the diglycosylated band. These results are discussed in relation to the diversity of scrapie and BSE strains.

http://jvi.asm.org/cgi/content/full/81/13/7230?view=long&pmid=17442721


In the US, scrapie is reported primarily in sheep homozygous for 136A/171Q (AAQQ) and the disease phenotype is similar to that seen with experimental strain CH1641.

http://www.ars.usda.gov/research/publications/publications.htm?seq_no_115=182469


snip...

please see full text ;



Sunday, December 12, 2010

EFSA reviews BSE/TSE infectivity in small ruminant tissues News Story 2 December 2010

http://transmissiblespongiformencephalopathy.blogspot.com/2010/12/efsa-reviews-bsetse-infectivity-in.html



Monday, November 22, 2010

Atypical transmissible spongiform encephalopathies in ruminants: a challenge for disease surveillance and control

REVIEW ARTICLES

http://transmissiblespongiformencephalopathy.blogspot.com/2010/11/atypical-transmissible-spongiform.html





Thursday, November 18, 2010

Increased susceptibility of human-PrP transgenic mice to bovine spongiform encephalopathy following passage in sheep

http://bse-atypical.blogspot.com/2010/11/increased-susceptibility-of-human-prp.html



Saturday, December 18, 2010

OIE Global Conference on Wildlife Animal Health and Biodiversity - Preparing for the Future (TSE AND PRIONS) Paris (France), 23-25 February 2011

http://transmissiblespongiformencephalopathy.blogspot.com/2010/12/oie-global-conference-on-wildlife.html



Scrapie

The two Commissions discussed the issue of ‘atypical’ scrapie in terms of notification requirements and the issue of the host genetic resistance. In response to questions of Members, the Code Commission clarified that ‘classical’ scrapie is reportable to the OIE but that ‘atypical’ scrapie is not reportable (in accordance with the recommendations made by the ad hoc Group on Atypical Scrapie and Atypical BSE, which met in November 2007). However, the sharing of scientific information on ‘atypical’ scrapie is encouraged. At this time, the Code Commission considered that more scientific information would be needed to fully address the issues associated with host genotype.

EU comment

4

OIE Terrestrial Animal Health Standards Commission / September 2010

The EU takes note of the fact that atypical scrapie is not an OIE listed disease. Nevertheless, it will remain notifiable in the EU. Moreover it must be stressed that any emergence of this disease should be notified to the OIE by Members and that scientific data should continue to be gathered.

snip...

Zoonotic Potential

Has transmission to humans been proven? (with the exception of artificial

circumstances) AND

Is human infection associated with severe consequences? (death or prolonged illness)

http://ec.europa.eu/food/international/organisations/docs/EU_comments_OIE_terrestrial_animal_health_code_en.pdf



Tuesday, November 02, 2010

BSE - ATYPICAL LESION DISTRIBUTION (RBSE 92-21367) statutory (obex only) diagnostic criteria CVL 1992

http://bse-atypical.blogspot.com/2010/11/bse-atypical-lesion-distribution-rbse.html



Friday, August 29, 2008

A C-Terminal Protease-Resistant Prion Fragment Distinguishes Ovine "CH1641-Like" Scrapie from Bovine Classical and L-Type BSE in Ovine Transgenic Mice

http://bse-atypical.blogspot.com/2008/08/c-terminal-protease-resistant-prion.html



Seven main threats for the future linked to prions

The NeuroPrion network has identified seven main threats for the future linked to prions.

First threat

The TSE road map defining the evolution of European policy for protection against prion diseases is based on a certain numbers of hypotheses some of which may turn out to be erroneous. In particular, a form of BSE (called atypical Bovine Spongiform Encephalopathy), recently identified by systematic testing in aged cattle without clinical signs, may be the origin of classical BSE and thus potentially constitute a reservoir, which may be impossible to eradicate if a sporadic origin is confirmed.

*** Also, a link is suspected between atypical BSE and some apparently sporadic cases of Creutzfeldt-Jakob disease in humans. These atypical BSE cases constitute an unforeseen first threat that could sharply modify the European approach to prion diseases.

http://www.neuroprion.org/en/np-neuroprion.html



Thursday, August 12, 2010

Seven main threats for the future linked to prions

http://prionpathy.blogspot.com/2010/08/seven-main-threats-for-future-linked-to.html


http://prionpathy.blogspot.com/


AS implied in the Inset 25 we must not _ASSUME_ that transmission of BSE to other species will invariably present pathology typical of a scrapie-like disease.

snip...

http://collections.europarchive.org/tna/20080102185948/http://www.bseinquiry.gov.uk/files/yb/1991/01/04004001.pdf



TSS

Wednesday, February 24, 2010

Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America

18.173 page 189

Experimental Challenge of Cattle with H-type and L-type Atypical BSE

A. Buschmann1, U. Ziegler1, M. Keller1, R. Rogers2, B. Hills3, M.H. Groschup1. 1Friedrich-Loeffler-Institut, Greifswald-Insel Riems, Germany, 2Health Canada, Bureau of Microbial Hazards, Health Products & Food Branch, Ottawa, Canada, 3Health Canada, Transmissible Spongiform Encephalopathy Secretariat, Ottawa, Canada

Background: After the detection of two novel BSE forms designated H-type and L-type atypical BSE the question of the pathogenesis and the agent distribution of these two types in cattle was fully open. From initial studies of the brain pathology, it was already known that the anatomical distribution of L-type BSE differs from that of the classical type where the obex region in the brainstem always displays the highest PrPSc concentrations. In contrast in L-type BSE cases, the thalamus and frontal cortex regions showed the highest levels of the pathological prion protein, while the obex region was only weakly involved.

Methods:We performed intracranial inoculations of cattle (five and six per group) using 10%brainstemhomogenates of the two German H- and L-type atypical BSE isolates. The animals were inoculated under narcosis and then kept in a free-ranging stable under appropriate biosafety conditions.At least one animal per group was killed and sectioned in the preclinical stage and the remaining animals were kept until they developed clinical symptoms. The animals were examined for behavioural changes every four weeks throughout the experiment following a protocol that had been established during earlier BSE pathogenesis studies with classical BSE.

Results and Discussion: All animals of both groups developed clinical symptoms and had to be euthanized within 16 months. The clinical picture differed from that of classical BSE, as the earliest signs of illness were loss of body weight and depression. However, the animals later developed hind limb ataxia and hyperesthesia predominantly and the head. Analysis of brain samples from these animals confirmed the BSE infection and the atypical Western blot profile was maintained in all animals. Samples from these animals are now being examined in order to be able to describe the pathogenesis and agent distribution for these novel BSE types. Conclusions: A pilot study using a commercially avaialble BSE rapid test ELISA revealed an essential restriction of PrPSc to the central nervous system for both atypical BSE forms. A much more detailed analysis for PrPSc and infectivity is still ongoing.


http://www.isid.org/14th_icid/


http://ww2.isid.org/Downloads/IMED2009_AbstrAuth.pdf


http://www.isid.org/publications/ICID_Archive.shtml





14th ICID International Scientific Exchange Brochure -

Final Abstract Number: ISE.114

Session: International Scientific Exchange

Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America

update October 2009

T. Singeltary

Bacliff, TX, USA

Background:

An update on atypical BSE and other TSE in North America. Please remember, the typical U.K. c-BSE, the atypical l-BSE (BASE), and h-BSE have all been documented in North America, along with the typical scrapie's, and atypical Nor-98 Scrapie, and to date, 2 different strains of CWD, and also TME. All these TSE in different species have been rendered and fed to food producing animals for humans and animals in North America (TSE in cats and dogs ?), and that the trading of these TSEs via animals and products via the USA and Canada has been immense over the years, decades.

Methods:

12 years independent research of available data

Results:

I propose that the current diagnostic criteria for human TSEs only enhances and helps the spreading of human TSE from the continued belief of the UKBSEnvCJD only theory in 2009. With all the science to date refuting it, to continue to validate this old myth, will only spread this TSE agent through a multitude of potential routes and sources i.e. consumption, medical i.e., surgical, blood, dental, endoscopy, optical, nutritional supplements, cosmetics etc.

Conclusion:

I would like to submit a review of past CJD surveillance in the USA, and the urgent need to make all human TSE in the USA a reportable disease, in every state, of every age group, and to make this mandatory immediately without further delay. The ramifications of not doing so will only allow this agent to spread further in the medical, dental, surgical arena's. Restricting the reporting of CJD and or any human TSE is NOT scientific. Iatrogenic CJD knows NO age group, TSE knows no boundaries. I propose as with Aguzzi, Asante, Collinge, Caughey, Deslys, Dormont, Gibbs, Gajdusek, Ironside, Manuelidis, Marsh, et al and many more, that the world of TSE Transmissible Spongiform Encephalopathy is far from an exact science, but there is enough proven science to date that this myth should be put to rest once and for all, and that we move forward with a new classification for human and animal TSE that would properly identify the infected species, the source species, and then the route.


http://ww2.isid.org/Downloads/14th_ICID_ISE_Abstracts.pdf




International Society for Infectious Diseases Web: http://www.isid.org/





Saturday, January 2, 2010

Human Prion Diseases in the United States January 1, 2010 ***FINAL***


http://prionunitusaupdate2008.blogspot.com/2010/01/human-prion-diseases-in-united-states.html



my comments to PLosone here ;


http://www.plosone.org/annotation/listThread.action?inReplyTo=info%3Adoi%2F10.1371%2Fannotation%2F04ce2b24-613d-46e6-9802-4131e2bfa6fd&root=info%3Adoi%2F10.1371%2Fannotation%2F04ce2b24-613d-46e6-9802-4131e2bfa6fd




Friday, February 05, 2010

New Variant Creutzfelt Jakob Disease case reports United States 2010 A Review


http://vcjd.blogspot.com/2010/02/new-variant-creutzfelt-jakob-disease.html



Sunday, February 14, 2010

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


http://bseusa.blogspot.com/2010/02/docket-no-fsis-2006-0011-fsis-harvard.html




Tuesday, March 16, 2010

COMMONWEALTH OF AUSTRALIA Hansard Import restrictions on beef FRIDAY, 5 FEBRUARY 2010 AUSTRALIA

COMMONWEALTH OF AUSTRALIA

Proof Committee Hansard




RRA&T 2 Senate Friday, 5 February 2010

RURAL AND REGIONAL AFFAIRS AND TRANSPORT

[9.03 am]

BELLINGER, Mr Brad, Chairman, Australian Beef Association

CARTER, Mr John Edward, Director, Australian Beef Association

CHAIR—Welcome. Would you like to make an opening statement?

Mr Bellinger—Thank you. The ABA stands by its submission, which we made on 14 December last year, that the decision made by the government to allow the importation of beef from BSE affected countries is politically based, not science based. During this hearing we will bring forward compelling new evidence to back up this statement. When I returned to my property after the December hearing I received a note from an American citizen. I will read a small excerpt from the mail he sent me in order to reinforce the dangers of allowing the importation of beef from BSE affected countries. I have done a number of press releases on this topic, and this fellow has obviously picked my details up from the internet. His name is Terry Singeltary and he is from Bacliff, Texas. He states, and rightfully so:

You should be worried. Please let me explain. I’ve kept up with the mad cow saga for 12 years today, on December 14th 1997, some four months post voluntary and partial mad cow feed ban in the USA, I lost my mother to the Heidenhain variant Creutzfeldt-Jakob disease (CJD). I know this is just another phenotype of the infamous sporadic CJDs. Here in the USA, when USA sheep scrapie was transmitted to USA bovine, the agent was not UK BSE—it was a different strain. So why then would human TSE from USA cattle look like UK CJD from UK BSE? It would not. So this accentuates that the science is inconclusive still on this devastating disease. He goes on to state:

The OIE— the International Organisation of Epizootics, the arm of the WTO— is a failed global agent that in my opinion is bought off via bogus regulations for global trade and industry reps. I have done this all these years for nothing but the truth. I am a consumer, I eat meat, but I do not have to sit idly by and see the ignorance and greed of it all while countless numbers of humans and animals are being exposed to the TSE agents. All the USA is interested in is trade, nothing else matters.

Even Dr Stanley Prusiner, who incidentally won the Nobel Health Prize in 1997 for his work on the prion—he invented the word ‘prion’, or it came from him—states:

The BSC policy was set up for one purpose only, trade—the illegal trading of all strains of TSE globally throughout North America, which is home to CBSC, IBSC and HBSC, many scrapie strains and two strains of CJD to date. (please note typo error, those should have read cBSE, lBSE, and hBSE...tss)

I would also like, while I have the opportunity, to explain the beef-off-the-shelves myth. At the first Senate hearing on 14 December, it was explained that the reason why they allowed BSC beef into Australia was the beef-off-the-shelves policy, whereby if we found a case of BSC in Australia they would have to recall all—

Friday, 5 February 2010 Senate RRA&T 3

RURAL AND REGIONAL AFFAIRS AND TRANSPORT

Senator HEFFERNAN—Which of course is total BS.

Mr Bellinger—Correct. This is written in the FSANZ document—Food Standards Australia New Zealand. Why isn’t this same policy in New Zealand? It is not—it is only in Australia. We are the only country in the world to have this idiotic policy. So we again call for the tabling of the WTO obligations paperwork. We do not believe that exists.



snip...see full text 110 pages ;





http://www.aph.gov.au/hansard/senate/commttee/S12742.pdf



for those interested, please see much more here ;



http://docket-aphis-2006-0041.blogspot.com/2010/03/commonwealth-of-australia-hansard.html





TSS