Thursday, November 25, 2010

Detection of the Abnormal Isoform of the Prion Protein Associated With Chronic Wasting Disease in the Optic Pathways of the Brain and Retina of Rocky

Detection of the Abnormal Isoform of the Prion Protein Associated With Chronic Wasting Disease in the Optic Pathways of the Brain and Retina of Rocky Mountain Elk (Cervus elaphus nelsoni)

T. R. Spraker1, K. I. O’Rourke2, T. Gidlewski3, J. G. Powers4, J. J. Greenlee5, and M. A. Wild4 Abstract Eyes and nuclei of the visual pathways in the brain were examined in 30 Rocky Mountain elk (Cervus elaphus nelsoni) representing 3 genotypes of the prion protein gene PRNP (codon 132: MM, ML, or LL).

Tissues were examined for the presence of the abnormal isoform of the prion protein associated with chronic wasting disease (PrPCWD). Nuclei and axonal tracts from a single section of brain stem at the level of the dorsal motor nucleus of the vagus nerve were scored for intensity and distribution of PrPCWD immunoreactivity and degree of spongiform degeneration. This obex scoring ranged from 0 (elk with no PrPCWD in the brain stem) to 10 (representing elk in terminal stage of disease). PrPCWD was detected in the retina of 16 of 18 (89%) elk with an obex score of > 7. PrPCWD was not detected in the retina of the 3 chronic wasting disease–negative elk and 9 elk with an obex score of < 6. PrPCWD was found in the nuclei of the visual pathways in the brain before it was found in the retina. Within the retina, PrPCWD was first found in the inner plexiform layer, followed by the outer plexiform layer. Intracytoplasmic accumulation of PrPCWD was found in a few neurons in the ganglion cell layer in the PRNP 132ML elk but was a prominent feature in the PRNP 132LL elk. Small aggregates of PrPCWD were present on the inner surface of the outer limiting membrane in PRNP 132LL elk but not in PRNP 132MM or 132ML elk. This study demonstrates PrPCWD accumulation in nuclei of the visual pathways of the brain, followed by PrPCWD in the retina.

Keywords brain, chronic wasting disease, eyes, prion protein, retina, Rocky Mountain elk, visual pathways

http://www.aphis.usda.gov/wildlife_damage/nwdp/pdf/Spraker%20et%20al%202010.pdf


PPo2-27:

Generation of a Novel form of Human PrPSc by Inter-species Transmission of Cervid Prions

Marcelo A. Barria,1 Glenn C. Telling,2 Pierluigi Gambetti,3 James A. Mastrianni4 and Claudio Soto1 1Mitchell Center for Alzheimer’s disease and related Brain disorders; Dept of Neurology; University of Texas Houston Medical School; Houston, TX USA; 2Dept of Microbiology, Immunology & Molecular Genetics and Neurology; Sanders Brown Center on Aging; University of Kentucky Medical Center; Lexington, KY USA; 3Institute of Pathology; Case western Reserve University; Cleveland, OH USA; 4Dept of Neurology; University of Chicago; Chicago, IL USA

Prion diseases are infectious neurodegenerative disorders affecting humans and animals that result from the conversion of normal prion protein (PrPC) into the misfolded and infectious prion (PrPSc). Chronic wasting disease (CWD) of cervids is a prion disorder of increasing prevalence within the United States that affects a large population of wild and captive deer and elk. CWD is highly contagious and its origin, mechanism of transmission and exact prevalence are currently unclear. The risk of transmission of CWD to humans is unknown. Defining that risk is of utmost importance, considering that people have been infected by animal prions, resulting in new fatal diseases. To study the possibility that human PrPC can be converted into the infectious form by CWD PrPSc we performed experiments using the Protein Misfolding Cyclic Amplification (PMCA) technique, which mimic in vitro the process of prion replication. Our results show that cervid PrPSc can induce the pathological conversion of human PrPC, but only after the CWD prion strain has been stabilized by successive passages in vitro or in vivo. Interestingly, this newly generated human PrPSc exhibits a distinct biochemical pattern that differs from any of the currently known forms of human PrPSc, indicating that it corresponds to a novel human prion strain. Our findings suggest that CWD prions have the capability to infect humans, and that this ability depends on CWD strain adaptation, implying that the risk for human health progressively increases with the spread of CWD among cervids.

PPo3-7:

Prion Transmission from Cervids to Humans is Strain-dependent

Qingzhong Kong, Shenghai Huang,*Fusong Chen, Michael Payne, Pierluigi Gambetti and Liuting Qing Department of Pathology; Case western Reserve University; Cleveland, OH USA *Current address: Nursing Informatics; Memorial Sloan-Kettering Cancer Center; New York, NY USA

Key words: CWD, strain, human transmission

Chronic wasting disease (CWD) is a widespread prion disease in cervids (deer and elk) in North America where significant human exposure to CWD is likely and zoonotic transmission of CWD is a concern. Current evidence indicates a strong barrier for transmission of the classical CWD strain to humans with the PrP-129MM genotype. A few recent reports suggest the presence of two or more CWD strains. What remain unknown is whether individuals with the PrP-129VV/MV genotypes are also resistant to the classical CWD strain and whether humans are resistant to all natural or adapted cervid prion strains. Here we report that a human prion strain that had adopted the cervid prion protein (PrP) sequence through passage in cervidized transgenic mice efficiently infected transgenic mice expressing human PrP, indicating that the species barrier from cervid to humans is prion strain-dependent and humans can be vulnerable to novel cervid prion strains. Preliminary results on CWD transmission in transgenic mice expressing human PrP-129V will also be discussed.

Acknowledgement Supported by NINDS NS052319 and NIA AG14359.



Wednesday, September 08, 2010


CWD PRION CONGRESS SEPTEMBER 8-11 2010

http://chronic-wasting-disease.blogspot.com/2010/09/cwd-prion-2010.html


http://chronic-wasting-disease.blogspot.com/




The Heidenhain Variant of Creutzfeldt-Jakob Disease

Stefan Kropp, MD; Walter J. Schulz-Schaeffer, MD; Michael Finkenstaedt, MD; Christian Riedemann, MD; Otto Windl, PhD; Bernhard J. Steinhoff, MD; Inga Zerr, MD; Hans A. Kretzschmar, MD; Sigrid Poser, MD

Arch Neurol. 1999;56:55-61.

Objective To investigate whether typical neuropathological and radiological findings can be identified in patients with the clinical diagnosis of the Heidenhain variant of Creutzfeldt-Jakob disease (CJD).

Design Case study. The clinical symptoms, neuropathological findings, electroencephalograms, magnetic resonance images, and cerebrospinal fluid samples of 14 Heidenhain cases were evaluated. Neuropathological changes were compared with those in a group of 14 patients with ataxia as the leading clinical sign.

Setting A university hospital, base of the German National Creutzfeldt-Jakob Disease Surveillance Study.

Patients Medical records of 169 neurologically examined patients with prospectively classified and neuropathologically confirmed CJD were analyzed.

Main Outcome Measure Difference in neuropathological and radiological findings between patients with the Heidenhain variant and other patients with CJD.

Results Of 169 patients with confirmed CJD, 20% showed characteristic clinical findings such as blurred vision, visual field restriction, metamorphopsia, or cortical blindness. Disease course of the Heidenhain group, as compared with the group of all patients with definite CJD, was significantly shorter (5.7 months vs 7.5 months; P=.02, t test). Neuropathological examination of patients with the Heidenhain variant showed most pronounced changes in the occipital lobe but less damage in the cingulate gyrus and basal ganglia compared with 14 patients with CJD who had ataxia as the leading clinical sign. Eleven (92%) of 12 genetically analyzed Heidenhain cases were homozygous for methionine at codon 129 of the prion protein gene (PRNP). In 9 of 9 cases, the 14-3-3 protein was present. In 7 (78%) of 9 cases, the level of neuron-specific enolase was elevated, with a concentration above 35 ng/mL. Periodic sharp-wave complexes were observed in 11 (78%) of the 14 cases. In 7 (63%) of 11 patients, magnetic resonance images showed symmetric hyperintensities in the basal ganglia in the T2- and proton-weighted sequence. In 4 of 11 cases the T2- and proton density–weighted images showed a pronounced signal increase confined to the gray matter of the occipital and visual cortex. Isolated atrophy of the visual cortex was noticeable in 2 of 11 cases.

Conclusions The clinical presentation of the Heidenhain variant of CJD was shown to correlate with the neuropathological findings of gliosis and nerve cell loss. In patients with visual disorders of unclear origin and signs of dementia, the differential diagnosis of a Heidenhain variant of CJD must be taken into consideration.

From the Departments of Neurology (Drs Kropp, Riedemann, Zerr, and Poser), Neuropathology (Drs Schulz-Schaeffer, Windl, and Kretzschmar), Neuroradiology (Dr Finkenstaedt), and Clinical Neurophysiology (Dr Steinhoff), Georg-August-University Göttingen, Göttingen, and the MR/CT Institute Hamburg, Hamburg (Dr Finkenstaedt), Germany.

http://archneur.ama-assn.org/cgi/content/abstract/56/1/55


full text pdf ;

http://archneur.ama-assn.org/cgi/reprint/56/1/55.pdf


Monday, December 14, 2009

Similarities between Forms of Sheep Scrapie and Creutzfeldt-Jakob Disease Are Encoded by Distinct Prion Types

(hmmm, this is getting interesting now...TSS)

Sporadic CJD type 1 and atypical/ Nor98 scrapie are characterized by fine (reticular) deposits,

see also ;

All of the Heidenhain variants were of the methionine/ methionine type 1 molecular subtype.

http://cjdusa.blogspot.com/2009/09/co-existence-of-scrapie-prion-protein.html


see full text ;

Monday, December 14, 2009

Similarities between Forms of Sheep Scrapie and Creutzfeldt-Jakob Disease Are Encoded by Distinct Prion Types

http://nor-98.blogspot.com/2009/12/similarities-between-forms-of-sheep.html


Heidenhain Variant Creutzfeldt Jakob Disease autopsy case report 'MOM'

DIVISION OF NEUROPATHOLOGY University of Texas Medical Branch 114 McCullough Bldg. Galveston, Texas 77555-0785

FAX COVER SHEET

DATE: 4-23-98

TO: Mr. Terry Singeltary @ -------

FROM: Gerald Campbell

FAX: (409) 772-5315 PHONE: (409) 772-2881

Number of Pages (including cover sheet):

Message:

*CONFIDENTIALITY NOTICE*

snip...see full text ;

http://creutzfeldt-jakob-disease.blogspot.com/2008/07/heidenhain-variant-creutzfeldt-jakob.html


Friday, August 27, 2010

NEW ATYPICAL NOR-98 SCRAPIE CASE DETECTED IDAHO NOW 5 CASES DOCUMENTED 2010

http://nor-98.blogspot.com/2010/08/new-atypical-nor-98-scrapie-case.html


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


Scrapie USA

http://scrapie-usa.blogspot.com/


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


Wednesday, September 08, 2010

CWD PRION CONGRESS SEPTEMBER 8-11 2010 PRION 2010

International Prion Congress: From agent to disease September 8–11, 2010 Salzburg, Austria

http://chronic-wasting-disease.blogspot.com/2010/09/cwd-prion-2010.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

UNITED STATES OF AMERICA VS GALEN J. NIEHUES FAKED MAD COW FEED TEST ON 92 BSE INSPECTION REPORTS FOR APPROXIMATELY 100 CATTLE OPERATIONS

http://bse-atypical.blogspot.com/2010/11/united-states-of-america-vs-galen-j.html


Tuesday, November 02, 2010

IN CONFIDENCE ''NEED TO KNOW''

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


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.

Second threat

In small ruminants, a new atypical form of scrapie currently represents up to 50% of detected cases and even involves sheep selected for resistance to classical scrapie. The consequences for animal and human health are still unknown and there may be a potential connection with atypical BSE. These atypical scrapie cases constitute a second threat not envisioned previously which could deeply modify the European approach to prion diseases.

Third threat

The species barrier between human and cattle might be weaker than previously expected and the risk of transmission of prion diseases between different species has been notoriously unpredictable. The emergence of new atypical strains in cattle and sheep together with the spread of chronic wasting disease in cervids renders the understanding of the species barrier critical. This constitutes a third threat not properly envisioned previously that could deeply modify the European approach to prion diseases.

Fourth threat

Prion infectivity has now been detected in blood, urine and milk and this has potential consequences on risk assessments for the environment and food as well as for contamination of surfaces including medical instruments. Furthermore the procedures recommended for decontamination of MBM (Meat and Bone Meal), which are based on older methodologies not designed for this purpose, have turned out to be of very limited efficacy and compromise current policies concerning the reuse of these high value protein supplements (cross-contamination of feed circuits are difficult to control). It should be noted that the destruction or very limited use of MBM is estimated to still cost 1 billion euros per year to the European economy,

whereas other countries, including the US,

Brazil, and Argentine do not have these constraints.

However, many uncertainties remain concerning the guarantees that can be reasonably provided for food and feed safety and scientific knowledge about the causative agents (prions) will continue to evolve. This decontamination and environmental issue is a fourth threat that could modify deeply the European approach to prion diseases.

Fifth threat The precise nature of prions remains elusive. Very recent data indicate that abnormal prion protein (PrPTSE) can be generated from the brains of normal animals, and under some conditions (including contaminated waste water) PrPTSE can be destroyed whereas the BSE infectious titre remains almost unchanged, a finding that underlines the possibility of having BSE without any detectable diagnostic marker. These are just two areas of our incomplete knowledge of the fundamental biology of prions which constitute a fifth threat to the European approach to prion diseases.

Sixth threat The absence of common methods and standardisation in the evaluation of multiple in vivo models with different prion strains and different transgenic mice expressing PrP from different species (different genotypes of cattle, sheep, cervids, etc) renders a complete and comprehensive analysis of all the data generated by the different scientific groups almost impossible. This deeply impairs risk assessment. Moreover, the possibility of generating PrPTSE de novo with new powerful techniques has raised serious questions about their appropriateness for use as blood screening tests. The confusion about an incorrect interpretation of positive results obtained by these methods constitutes a sixth threat to European approach to prion diseases.

Seventh Threat The detection of new or re-emerging prion diseases in animals or humans which could lead to a new crisis in consumer confidence over the relaxation of precautionary measures and surveillance programmes constitutes a seventh threat that could 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/


ALABAMA MAD COW g-h-BSEalabama

In this study, we identified a novel mutation in the bovine prion protein gene (Prnp), called E211K, of a confirmed BSE positive cow from Alabama, United States of America. This mutation is identical to the E200K pathogenic mutation found in humans with a genetic form of CJD. This finding represents the first report of a confirmed case of BSE with a potential pathogenic mutation within the bovine Prnp gene. We hypothesize that the bovine Prnp E211K mutation most likely has caused BSE in "the approximately 10-year-old cow" carrying the E221K mutation.

http://www.plospathogens.org/article/info%3Adoi%2F10.1371%2Fjournal.ppat.1000156


http://www.plospathogens.org/article/fetchObjectAttachment.action?uri=info%3Adoi%2F10.1371%2Fjournal.ppat.1000156&representation=PDF


Saturday, August 14, 2010

BSE Case Associated with Prion Protein Gene Mutation (g-h-BSEalabama) and VPSPr PRIONPATHY

(see mad cow feed in COMMERCE IN ALABAMA...TSS)

http://prionpathy.blogspot.com/2010/08/bse-case-associated-with-prion-protein.html


Wednesday, July 28, 2010

re-Freedom of Information Act Project Number 3625-32000-086-05, Study of Atypical BSE UPDATE July 28, 2010

http://bse-atypical.blogspot.com/2010/07/re-freedom-of-information-act-project.html


Saturday, November 6, 2010

TAFS1 Position Paper on Position Paper on Relaxation of the Feed Ban in the EU Berne, 2010 TAFS

INTERNATIONAL FORUM FOR TRANSMISSIBLE ANIMAL DISEASES AND FOOD SAFETY a non-profit Swiss Foundation

http://madcowfeed.blogspot.com/2010/11/tafs1-position-paper-on-position-paper.html


Monday, August 9, 2010

Variably protease-sensitive prionopathy: A new sporadic disease of the prion protein or just more PRIONBALONEY ?

http://prionunitusaupdate2008.blogspot.com/2010/08/variably-protease-sensitive-prionopathy.html


PLEASE SEE the dramatic increase in sporadic CJD cases in documented BSE countries,

TOTAL CASES OF SPORADIC CJD (DEATHS) DEFINITE AND PROBABLE CASES

Australia Austria Canada France Germany Italy Netherlands Slovakia Spain Switzerland UK

http://www.eurocjd.ed.ac.uk/sporadic.htm


USA

5 Includes 16 cases in which the diagnosis is pending, and 18 inconclusive cases;

6 Includes 21 (19 from 2010) cases with type determination pending in which the diagnosis of vCJD has been excluded.

2010

PLEASE NOTE REFERENCE LINES 5. AND 6.

Monday, August 9, 2010

National Prion Disease Pathology Surveillance Center Cases Examined (July 31, 2010) Year Total Referrals2 Prion Disease Sporadic Familial Iatrogenic vCJD

1996 & earlier 51 33 28 5 0 0

1997 114 68 59 9 0 0

1998 88 52 44 7 1 0

1999 120 72 64 8 0 0

2000 146 103 89 14 0 0

2001 209 119 109 10 0 0

2002 248 149 125 22 2 0

2003 274 176 137 39 0 0

2004 325 186 164 21 0 1(3)

2005 344 194 157 36 1 0

2006 383 197 166 29 0 2(4)

2007 377 214 187 27 0 0

2008 394 231 204 25 0 0

2009 425 259 216 43 0 0

2010 204 124 85 20 0 0

TOTAL 3702(5) 2177(6) 1834 315 4 3

1 Listed based on the year of death or, if not available, on year of referral;

2 Cases with suspected prion disease for which brain tissue and/or blood (in familial cases) were submitted;

3 Disease acquired in the United Kingdom;

4 Disease was acquired in the United Kingdom in one case and in Saudi Arabia in the other case;

5 Includes 16 cases in which the diagnosis is pending, and 18 inconclusive cases;

6 Includes 21 (19 from 2010) cases with type determination pending in which the diagnosis of vCJD has been excluded.

http://www.cjdsurveillance.com/pdf/case-table.pdf


Monday, August 9, 2010

National Prion Disease Pathology Surveillance Center Cases Examined (July 31, 2010)

(please watch and listen to the video and the scientist speaking about atypical BSE and sporadic CJD and listen to Professor Aguzzi)

http://prionunitusaupdate2008.blogspot.com/2010/08/national-prion-disease-pathology.html


Atypical BSE in Cattle

BSE has been linked to the human disease variant Creutzfeldt Jakob Disease (vCJD). The known exposure pathways for humans contracting vCJD are through the consumption of beef and beef products contaminated by the BSE agent and through blood transfusions. However, recent scientific evidence suggests that the BSE agent may play a role in the development of other forms of human prion diseases as well. These studies suggest that classical type of BSE may cause type 2 sporadic CJD and that H-type atypical BSE is connected with a familial form of CJD.

To date the OIE/WAHO assumes that the human and animal health standards set out in the BSE chapter for classical BSE (C-Type) applies to all forms of BSE which include the H-type and L-type atypical forms. This assumption is scientifically not completely justified and accumulating evidence suggests that this may in fact not be the case. Molecular characterization and the spatial distribution pattern of histopathologic lesions and immunohistochemistry (IHC) signals are used to identify and characterize atypical BSE. Both the L-type and H-type atypical cases display significant differences in the conformation and spatial accumulation of the disease associated prion protein (PrPSc) in brains of afflicted cattle. Transmission studies in bovine transgenic and wild type mouse models support that the atypical BSE types might be unique strains because they have different incubation times and lesion profiles when compared to C-type BSE. When L-type BSE was inoculated into ovine transgenic mice and Syrian hamster the resulting molecular fingerprint had changed, either in the first or a subsequent passage, from L-type into C-type BSE. In addition, non-human primates are specifically susceptible for atypical BSE as demonstrated by an approximately 50% shortened incubation time for L-type BSE as compared to C-type. Considering the current scientific information available, it cannot be assumed that these different BSE types pose the same human health risks as C-type BSE or that these risks are mitigated by the same protective measures.

snip...see full text ;

http://www.prionetcanada.ca/detail.aspx?menu=5&dt=293380&app=93&cat1=387&tp=20&lk=no&cat2


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.

page 114 ;

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



TSS

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Monday, November 22, 2010

Mother to Offspring Transmission of Chronic Wasting Disease

PPo3-40:


Mother to Offspring Transmission of Chronic Wasting Disease

Candace K. Mathiason, Amy V. Nalls, Kelly Anderson, Jeanette Hayes-Klug, Nicholas Haley and Edward A. Hoover

Colorado State University, Department of Microbiology, Immunology and Pathology, Fort Collins, CO USA

Key words: Chronic wasting disease, vertical transmission, muntjac deer

We have developed a new cervid model in small Asian muntjac deer (Muntiacus reevesi) to study potential modes of vertical transmission of chronic wasting disease (CWD) from mother to offspring. Eight of eight (8/8) muntjac doe orally infected with CWD tested PrPCWD lymphoid positive by 4 months post infection. Six fawns were born to these CWD-infected doe. Six fawns were born to 6 CWD-infected doe; 4 of the fawns were non-viable. The viable fawns have been monitored for CWD infection by immunohistochemistry and sPMCA performed on serial tonsil and rectal lymphoid tissue biopsies. PrPCWD has been detected in one fawn as early as 40 days of age. Moreover, sPMCA performed on rectal lymphoid tissue has yield positive results on another fawn at 10 days of age. In addition, sPMCA assays have also demonstrated amplifiable prions in maternal placental (caruncule) and mammary tissue of the dam.

Additional pregnancy related fluids and tissues from the doe as well as tissue from the nonviable fawns are currently being probed for the presence of CWD. In summary, we have employed the muntjac deer model, to demonstrate for the first time the transmission of CWD from mother to offspring. These studies provide the foundation to investigate the mechanisms and pathways of maternal prion transfer.



PRION 2010 Meeting Report International Prion Congress: From agent to disease; September 8–11, 2010; Salzburg, Austria Volume 4, Issue 3 July/August/September 2010



http://www.landesbioscience.com/journals/prion/article/12764/




http://chronic-wasting-disease.blogspot.com/





TSS

Labels: , , ,

Wednesday, November 17, 2010

CWD Update 98 November 10, 2010

CWD Update 98

November 10, 2010

State and Provincial Updates

Wisconsin:

The following press release was issued on November 15, 2010 by the Wisconsin Department of Natural Resources (http://dnr.wi.gov/news/BreakingNews_Lookup.asp?id=1911):


DNR asks for hunters help on Ashland area deer disease surveillance

Contact(s): Davin Lopez (608) 267-2948 Peter Dunn 608-317-8417

ASHLAND, WI. –The Department of Natural Resources is asking Ashland and Bayfield county hunters to help with surveillance efforts to see if chronic wasting disease may be present in free-ranging, wild deer the area.

Sampling stations where hunters can bring deer for disease testing will be at the following locations on opening weekend Nov. 20 and 21.

Pearce’s Sausage Kitchen - 61327 Dalhstrom Road, Ashland

Angler’s All – 2803 Lakeshore Drive. E. Ashland

Woody’s Taxidermy – 1109 Vaughn Avenue, Ashland

Bayside Taxidermy – 1110 Lakeshore Drive, Ashland

Chequamegon Taxidermy – 73740 Strecker Road, Washburn

Brian Weber Processing – 29125 State Hwy 137, Ashland

Ino Bar – 19020 US Hwy 2, Ino

Washburn Holiday Station- 606 W. Bayfield St., Washburn

The Department of Agriculture, Trade and Consumer Protection (DATCP) indicated Thursday, Nov. 11, that preliminary-positive test results on a deer removed in October from a game farm southwest of Ashland indicated possible presence of chronic wasting disease. Confirmatory testing of the tissues is underway and must be completed before DATCP officials can make a final determination. DATCP is responsible for the regulation of deer farm operations.

In order to find out if the disease has also made its way into the adjoining wild deer herd, DNR will begin a disease surveillance effort immediately and continue through the nine day deer gun season within a 10 mile radius around the city of Ashland. DNR will send staff to four big game registration stations to collect tissue samples. DNR hopes to gather samples on every adult deer registered. Department staff is also working with local meat processors, taxidermists, and car kill deer contractors to collect samples.

"While we don’t have the final test results at this time (Monday, Nov.15) we feel it’s prudent to do the surveillance based upon the preliminary information," said Mike Zeckmeister, DNR northern region wildlife supervisor. "The upcoming deer season is really the best opportunity for local hunters to assist in rapidly and efficiently collecting these samples."

Wisconsin wildlife officials stress that this is the first time captive herd surveillance testing suggests CWD may be present on a farm in northern Wisconsin. Two rounds of testing in wild deer since 2002 have found all wild deer healthy in northern Wisconsin to date.

In October, local conservation wardens completed a fence inspection on the farm as part of a land sale. During this inspection wardens found several breaches in the fence and indications that deer may have moved in and out of the farm.

"Wardens are continuing to inspect the fence and work with the farmer to ensure that the fence meets DNR specifications," said Dave Zebro, DNR Northern Region conservation warden supervisor.

"The possibility that free ranging deer may have been exposed to the disease is why we feel additional local disease surveillance is very important. We’re counting on help from the hunters to get the needed samples" Zeckmeister said.

The World Health Organization stresses that there is no known link between CWD in deer and the human version of this prion disease, however, people should no eat any deer that tests positive for CWD, appears sick or is acting strangely. Officials request that people report all such deer to a DNR biologist or warden.

Hunters supplying deer tissue samples for testing will be able to track test results for their deer on the department’s website: dnr.wi.gov. Test results will take three to four weeks to be posted.

Wisconsin:

The Wisconsin Department of Natural Resources also recently finalized their new "Wisconsin’s Chronic Wasting Disease Response Plan: 2010–2025." The plan can be viewed at: http://dnr.wi.gov/org/land/wildlife/whealth/issues/CWD/plan.htm.


New York:

Since the discovery of two white-tailed deer with CWD in 2005, the New York Department of Environmental Conservation (DEC) has found no additional cases of the disease. Subsequently, they have "decommissioned" their CWD containment area. CWD surveillance will continue in the state, and carcass import restrictions still apply. Additional information is available on the DEC website at: http://www.dec.ny.gov/outdoor/8325.html.


Recent Publications

Environmental Sources of Scrapie Prions

Ben C. Maddison, Claire A. Baker, Linda A. Terry, Susan J. Bellworthy, Leigh Thorne, Helen C. Rees, and Kevin C. Gough

Journal of Virology, November 2010, p. 11560-11562, Vol. 84, No. 21.

Abstract

Ovine scrapie and cervine chronic wasting disease show considerable horizontal transmission. Here we report that a scrapie-affected sheep farm has a widespread environmental contamination with prions. Prions were amplified by protein-misfolding cyclic amplification (sPMCA) from seven of nine environmental swab samples taken, including those from metal, plastic, and wooden surfaces. Sheep had been removed from the areas from which the swabs were taken up to 20 days prior to sampling, indicating that prions persist for at least that long. These data implicate inanimate objects as environmental reservoirs for prion infectivity that are likely to contribute to facile disease transmission.

http://jvi.asm.org/cgi/content/abstract/84/21/11560.


Experimental oral transmission of chronic wasting disease to red deer (Cervus elaphus elaphus): Early detection and late stage distribution of protease-resistant prion protein

Aru Balachandran, Noel P. Harrington, James Algire, Andrei Soutyrine, Terry R. Spraker, Martin Jeffrey, Lorenzo González, and Katherine I. O’Rourke

Can Vet J. 2010 February; 51(2): 169–178.

Abstract

Chronic wasting disease (CWD), an important emerging prion disease of cervids, is readily transmitted by intracerebral or oral inoculation from deer-to-deer and elk-to-elk, suggesting the latter is a natural route of exposure. Studies of host range susceptibility to oral infection, particularly of those species found in habitats where CWD currently exists are imperative. This report describes the experimental transmission of CWD to red deer following oral inoculation with infectious CWD material of elk origin. At 18 to 20 months post-inoculation, mild to moderate neurological signs and weight loss were observed and animals were euthanized and tested using 3 conventional immunological assays. The data indicate that red deer are susceptible to oral challenge and that tissues currently used for CWD diagnosis show strong abnormal prion (PrPCWD) accumulation. Widespread peripheral PrPCWD deposition involves lymphoreticular tissues, endocrine tissues, and cardiac muscle and suggests a potential source of prion infectivity, a means of horizontal transmission and carrier state.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2808282/


Estimating Chronic Wasting Disease Effects on Mule Deer Recruitment and Population Growth

Jessie Dulberger, N. Thompson Hobbs, Heather M. Swanson, Chad J. Bishop, and Michael W. Miller

Journal of Wildlife Diseases, 46(4), 2010, pp. 1086–1095.

Abstract

Chronic wasting disease (CWD), a prion disease of mule deer (Odocoileus hemionus), accelerates mortality and in so doing has the potential to influence population dynamics. Although effects on mule deer survival are clear, how CWD affects recruitment is less certain. We studied how prion infection influenced the number of offspring raised to weaning per adult (=2 yr old) female mule deer and subsequently the estimated growth rate (?) of an infected deer herd. Infected and presumably uninfected radio-collared female deer were observed with their fawns in late summer (August–September) during three consecutive years (2006–2008) in the Table Mesa area of Boulder, Colorado, USA. We counted the number of fawns accompanying each female, then used a fully Bayesian model to estimate recruitment by infected and uninfected females and the effect of the disease on ?. On average, infected females weaned 0.95 fawns (95% credible interval = 0.56–1.43) whereas uninfected females weaned 1.34 fawns (95% credible interval = 1.09–1.61); the probability that uninfected females weaned more fawns than infected females was 0.93). We used estimates of prevalence to weight recruitment and survival parameters in the transition matrix of a three-age, single-sex matrix model and then used the matrix to calculate effects of CWD on ?. When effects of CWD on both survival and recruitment were included, the modeled ? was 0.97 (95% credible interval = 0.82–1.09). Effects of disease on ? were mediated almost entirely by elevated mortality of infected animals. We conclude that although CWD may affect mule deer recruitment, these effects seem to be sufficiently small that they can be omitted in estimating the influences of CWD on population growth rate.

http://www.jwildlifedis.org/cgi/content/abstract/46/4/1086.


Prion Strain Mutation Determined by Prion Protein Conformational Compatibility and Primary Structure

Rachel C. Angers, Hae-Eun Kang, Dana Napier, Shawn Browning, Tanya Seward, Candace Mathiason, Aru Balachandran, Debbie McKenzie, Joaquín Castilla, Claudio Soto, Jean Jewell, Catherine Graham, Edward A. Hoover, Glenn C. Telling

Science 28 May 2010:Vol. 328. no. 5982, pp. 1154 - 1158

Abstract

Prions are infectious proteins composed of the abnormal disease-causing isoform PrPSc, which induces conformational conversion of the host-encoded normal cellular prion protein PrPC to additional PrPSc. The mechanism underlying prion strain mutation in the absence of nucleic acids remains unresolved. Additionally, the frequency of strains causing chronic wasting disease (CWD), a burgeoning prion epidemic of cervids, is unknown. Using susceptible transgenic mice, we identified two prevalent CWD strains with divergent biological properties but composed of PrPSc with indistinguishable biochemical characteristics. Although CWD transmissions indicated stable, independent strain propagation by elk PrPC, strain coexistence in the brains of deer and transgenic mice demonstrated unstable strain propagation by deer PrPC. The primary structures of deer and elk prion proteins differ at residue 226, which, in concert with PrPSc conformational compatibility, determines prion strain mutation in these cervids.

http://www.sciencemag.org/cgi/content/abstract/328/5982/1154.


Chronic Wasting Disease (CWD) Susceptibility of Several North American Rodents That Are Sympatric with Cervid CWD Epidemics

Dennis M. Heisey, Natalie A. Mickelsen, Jay R. Schneider, Christopher J. Johnson, Chad J. Johnson, Julia A. Langenberg, Philip N. Bochsler, Delwyn P. Keane, and Daniel J. Barr

Journal of Virology, January 2010, p. 210-215, Vol. 84, No. 1.

Abstract

Chronic wasting disease (CWD) is a highly contagious always fatal neurodegenerative disease that is currently known to naturally infect only species of the deer family, Cervidae. CWD epidemics are occurring in free-ranging cervids at several locations in North America, and other wildlife species are certainly being exposed to infectious material. To assess the potential for transmission, we intracerebrally inoculated four species of epidemic-sympatric rodents with CWD. Transmission was efficient in all species; the onset of disease was faster in the two vole species than the two Peromyscus spp. The results for inocula prepared from CWD-positive deer with or without CWD-resistant genotypes were similar. Survival times were substantially shortened upon second passage, demonstrating adaptation. Unlike all other known prion protein sequences for cricetid rodents that possess asparagine at position 170, our red-backed voles expressed serine and refute previous suggestions that a serine in this position substantially reduces susceptibility to CWD. Given the scavenging habits of these rodent species, the apparent persistence of CWD prions in the environment, and the inevitable exposure of these rodents to CWD prions, our intracerebral challenge results indicate that further investigation of the possibility of natural transmission is warranted.

http://jvi.asm.org/cgi/content/abstract/84/1/210



Influence of genetic relatedness and spatial proximity on chronic wasting disease infection among female white-tailed deer

Daniel A. Grear, Michael D. Samuel, Kim T. Scribner, Byron V. Weckworth, Julie A. Langenberg

Journal of Applied Ecology: Volume 47, Issue 3, pages 532–540, June 2010

Abstract

1. Social organization and interactions among individuals are suspected to play important roles in the transmission and potential management of wildlife diseases. However, few studies have been conducted to evaluate sociality in wildlife disease transmission. We evaluated the hypothesis of socially facilitated transmission of chronic wasting disease (CWD) among adult female white-tailed deer using spatial location and genetic relatedness for 1387 female deer, and spatial locations of 1321 adult male deer harvested during 2002–2004 CWD control efforts in Wisconsin, USA.

2. Genetically related female deer were significantly clustered at distances of <3·2 km. However, spatial autocorrelation based on maternally inherited mitochondrial DNA was 50-fold higher than relatedness estimated from microsatellite loci, indicating spatial overlap of females from different social groups with high rates of male-mediated dispersal and gene flow among groups.

3. Probability of CWD infection in adult females was significantly increased by closely related (full-sibling, mother-offspring) infected females that were both spatially proximate (=3.2 km) and farther distant. To a minor extent, the probability of infection was also influenced by the number of nearby infected females (=3.2 km), but not by the number of infected males.

4. Direct deer-to-deer transmission of CWD between closely related female deer may be an important route of local CWD transmission.

5. Synthesis and applications. Random mixing and infectious contact may be inadequate models for CWD transmission and disease spread in female deer. Frequency-dependent CWD transmission may be important for females because infectious contacts are limited between members of different female social groups, even if ranges overlap. Given that our data demonstrate a strong relationship between infection probability and female relatedness, CWD management should consider female harvest to maintain smaller female social groups and reduce contact among female deer. However, evaluation of the effects of this strategy on deer social behaviour and contact is needed.


http://onlinelibrary.wiley.com/doi/10.1111/j.1365-2664.2010.01813.x/abstract


Human Dimensions of Wildlife

http://www.tandf.co.uk/journals/titles/10871209.asp

Volume 15, Issue 3, 2010 of this journal was dedicated to Chronic Wasting Disease.

Below are selected abstracts from this volume.

CWD After "the Fire": Six Reasons Why Hunters Resisted Wisconsin's Eradication Effort Robert H. Holsman; Jordan Petchenik; Erin E. Cooney Human Dimensions of Wildlife, Volume 15, Issue 3 May 2010, pages 180 - 193

Abstract

Eight years after undertaking an unprecedented attempt to eradicate chronic wasting disease (CWD) from its free-ranging white-tailed deer (Odocoileus virginianus) population, Wisconsin wildlife managers are rethinking their strategies in the face of public opposition to their efforts. This article draws on a dozen surveys of hunters and landowners to identify six psychological bases that created deer hunter opposition to the Wisconsin plan. These include opposition to the population goal, conflicts with traditions, conflicts with consumption norms, the uncertainty of the plan's efficacy, and perceived lack of credibility in the agency. We argue that these six clusters of attitudinal beliefs made it unlikely that hunter support could have been cultivated regardless of the scope or pace of the CWD eradication effort. Our findings call into question the use of recreational hunting as a viable tool for bringing about severe deer population reductions for disease management.

Influences on Hunter Support for Deer Herd Reduction as a Chronic Wasting Disease (CWD) Management Strategy

Erin E. Cooney; Robert H. Holsman

Human Dimensions of Wildlife, Volume 15, Issue 3 May 2010, pages 194 - 207

Abstract

The extent to which wildlife diseases like chronic wasting disease (CWD) are density dependent creates opportunities to manage them by implementing population reduction to disrupt disease spread and lower its prevalence. We tested a model to investigate the influence of risk perceptions and other salient beliefs on deer hunter support for deer density reduction as chronic wasting disease strategy in Wisconsin. We found that the influence of risk perceptions on hunter support for population goals was mediated through beliefs about whether eradication is necessary. Our results suggest that hunter beliefs about the likelihood of deer reduction achieving CWD eradication had the greatest influence on support for herd reduction. If managers intend to use recreational hunters to combat CWD, they need to provide tangible evidence that deer reduction results in progress in containing or eliminating CWD to increase beliefs in the efficacy of the strategy.

Predicting Hunting Participation in Response to Chronic Wasting Disease in Four States


Katie M. Lyon; Jerry J. Vaske Human Dimensions of Wildlife, Volume 15, Issue 3 May 2010, pages 208 - 220

Abstract


This article examines how factors related and unrelated to chronic wasting disease (CWD) influenced hunters to stop hunting deer. Data were obtained from a survey of resident and nonresident deer hunters in Arizona, North Dakota, South Dakota, and Wisconsin (n = 3,519). Hunters were presented with six hypothetical scenarios depicting increasing CWD prevalence levels and human impact (e.g., human death), and asked if they would continue or stop hunting deer in the state. A series of logistic regression models examined the influence of four dimensions of predictor variables: (a) prevalence, (b) human impact, (c) perceived risks from CWD, and (d) location of hunting participation (i.e., state, residency). Participation in deer hunting in these four states will decrease substantially if CWD prevalence increases dramatically. If high prevalence is combined with human death from CWD, the decline is even greater. Human impact and perceived risks had the largest effect on hunter behavior.


http://wildlifedisease.nbii.gov/documents/CWD%20Updates/update%2098.pdf



Aerosol and nasal transmission of chronic wasting disease in cervidized mice


Nathaniel D. Denkers1, Davis M. Seelig1, Glenn C. Telling2 and Edward A. Hoover1 1 Department of Microbiology, Immunology and Pathology, Colorado State University, Fort Collins, CO 80523-1619, USA 2 Department of Microbiology, Immunology and Molecular Genetics, Sanders Brown Center of Aging and Department of Neurology, University of Kentucky, Lexington, KY, USA Correspondence Edward A. Hoover edward.hoover@colostate.edu


Little is known regarding the potential risk posed by aerosolized prions. Chronic wasting disease (CWD) is transmitted horizontally, almost surely by mucosal exposure, and CWD prions are present in saliva and urine of infected animals. However, whether CWD may be transmissible by the aerosol or nasal route is not known. To address this question, FVB mice transgenetically expressing the normal cervid PrPC protein [Tg(cerPrP) mice] were exposed to CWD prions by either nose-only aerosol exposure or by drop-wise instillation into the nostrils. Mice were monitored for signs of disease for up to 755 days post-inoculation (p.i.) and by examination of tissues for lesions and PrPCWD after necropsy. In particular, nasal mucosa, vomeronasal organ, lungs, lymphoid tissue and the brain were assessed for PrPCWD by Western blotting and immunohistochemistry. Six of seven aerosol-exposed Tg(cerPrP) mice developed clinical signs of neurological dysfunction mandating euthanasia between 411 and 749 days p.i. In all these mice, CWD infection was confirmed by detection of spongiform lesions and PrPCWD in the brain. Two of nine intranasally inoculated Tg(cerPrP) mice also developed transmissible spongiform encephalopathy associated with PrPCWD between 417 and 755 days p.i. No evidence of PrPCWD was detected in CWD-inoculated Tg(cerPrP) mice examined at pre-terminal time points. These results demonstrate that CWD can be transmitted by aerosol (as well as nasal) exposure and suggest that exposure via the respiratory system merits consideration for prion disease transmission and biosafety.


http://vir.sgmjournals.org/cgi/content/abstract/91/6/1651


Saturday, November 13, 2010

CWD Infected buck found 40 miles from Michigan's U.P.


http://chronic-wasting-disease.blogspot.com/2010/11/infected-buck-found-40-miles-from.html


Friday, November 12, 2010

WHITE-TAILED BUCK HARVESTED NEAR MOORCROFT TESTS POSITIVE FOR CWD WYOMING

http://chronic-wasting-disease.blogspot.com/2010/11/white-tailed-buck-harvested-near.html



Sunday, October 31, 2010


Scientific Opinion on the results of the EU survey for Chronic Wasting Disease (CWD) in cervids EFSA Panel on Biological Hazards (BIOHAZ) (October) 2010


Greetings BSE-L members et al,

I would like to post the following about the EFSA Scientific opinion on CWD in cervids in the EU, and then, a review of sorts. let's take a look at past findings of TSE in the brains of different species over the past decades in the UK and the EU, and take a look at the testing blunders on brains, and here in the USA as well, and then ask yourself, were they really trying to find TSE, or not ??? IT's a lengthy post, i hope you find interesting. ...

kindest regards, terry


http://chronic-wasting-disease.blogspot.com/2010/10/scientific-opinion-on-results-of-eu.html



Sunday, April 12, 2009


CWD UPDATE Infection Studies in Two Species of Non-Human Primates and one Environmental reservoir infectivity study and evidence of two strains


snip...


From: TSS (216-119-163-189.ipset45.wt.net)

Subject: CWD aka MAD DEER/ELK TO HUMANS ???

Date: September 30, 2002 at 7:06 am PST

From: "Belay, Ermias"

To: Cc: "Race, Richard (NIH)" ;

; "Belay, Ermias"

Sent: Monday, September 30, 2002 9:22 AM

Subject: RE: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS

Dear Sir/Madam,


In the Archives of Neurology you quoted (the abstract of which was attached to your email), we did not say CWD in humans will present like variant CJD. That assumption would be wrong. I encourage you to read the whole article and call me if you have questions or need more clarification (phone: 404-639-3091).

Also, we do not claim that "no-one has ever been infected with prion disease from eating venison." Our conclusion stating that we found no strong evidence of CWD transmission to humans in the article you quoted or in any other forum is limited to the patients we investigated.


Ermias Belay, M.D. Centers for Disease Control and Prevention



-----Original Message-----

From: Sent: Sunday, September 29, 2002 10:15 AM

To: [log in to unmask]">[log in to unmask]; [log in to unmask]">[log in to unmask]; [log in to unmask]">[log in to unmask]

Subject: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS

Sunday, November 10, 2002 6:26 PM ......snip........end..............TSS

snip...

full text ;

http://chronic-wasting-disease.blogspot.com/2009/02/exotic-meats-usa-announces-urgent.html


Wednesday, March 18, 2009

Noah's Ark Holding, LLC, Dawson, MN RECALL Elk products contain meat derived from an elk confirmed to have CWD NV, CA, TX, CO, NY, UT, FL, OK RECALLS AND FIELD CORRECTIONS: FOODS CLASS II

http://chronic-wasting-disease.blogspot.com/2009/03/noahs-ark-holding-llc-dawson-mn-recall.html


see full text ;

http://chronic-wasting-disease.blogspot.com/2009/04/cwd-update-infection-studies-in-two.html


Thursday, September 30, 2010

Characterization of the Prion Protein in Human Urine*

http://creutzfeldt-jakob-disease.blogspot.com/2010/09/characterization-of-prion-protein-in.html


UPDATED DATA ON 2ND CWD STRAIN

Wednesday, September 08, 2010

CWD PRION CONGRESS SEPTEMBER 8-11 2010

http://chronic-wasting-disease.blogspot.com/2010/09/cwd-prion-2010.html


http://chronic-wasting-disease.blogspot.com/


Thursday, October 07, 2010

Experimental Transmission of H-type Bovine Spongiform Encephalopathy to Bovinized Transgenic Mice

http://bse-atypical.blogspot.com/2010/10/experimental-transmission-of-h-type.html


Sunday, October 3, 2010

Scrapie, Nor-98 atypical Scrapie, and BSE in sheep and goats North America, who's looking ?

http://nor-98.blogspot.com/2010/10/scrapie-nor-98-atypical-scrapie-and-bse.html


Monday, December 21, 2009

Distinct Molecular Signature of Bovine Spongiform Encephalopathy Prion in Pigs

http://madporcinedisease.blogspot.com/2009/12/distinct-molecular-signature-of-bovine.html


Thursday, October 15, 2009

The presence of neurological signs in pigs inoculated with BSE without detectable PrPd raises the possibility that the BSE agent may produce a prion disease in pigs that remains undetected by the current postmortem tests.

Transmissibility studies of vacuolar changes in the rostral colliculus of pigs

http://madporcinedisease.blogspot.com/2009/10/transmissibility-studies-of-vacuolar.html


Saturday, December 01, 2007

Phenotypic Similarity of Transmissible Mink Encephalopathy in Cattle and L-type Bovine Spongiform Encephalopathy in a Mouse Model Volume 13, Number 12–December 2007 Research

http://transmissible-mink-encephalopathy.blogspot.com/2007/12/phenotypic-similarity-of-transmissible.html


IN CONFIDENCE

BSE - ATYPICAL LESION DISTRIBUTION (RBSE 92-21367)


http://tna.europarchive.org/20080609145105/http://www.bseinquiry.gov.uk/files/yb/1993/03/14001001.pdf


please see full text ;


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


Saturday, November 6, 2010

TAFS1 Position Paper on Position Paper on Relaxation of the Feed Ban in the EU Berne, 2010

TAFS

INTERNATIONAL FORUM FOR TRANSMISSIBLE ANIMAL DISEASES AND FOOD SAFETY a non-profit Swiss Foundation


http://madcowfeed.blogspot.com/2010/11/tafs1-position-paper-on-position-paper.html


Monday, August 9, 2010

National Prion Disease Pathology Surveillance Center Cases Examined (July 31, 2010)

(please watch and listen to the video and the scientist speaking about atypical BSE and sporadic CJD and listen to Professor Aguzzi)


http://prionunitusaupdate2008.blogspot.com/2010/08/national-prion-disease-pathology.html




TSS

Labels: , , , , ,

Saturday, November 13, 2010

CWD Infected buck found 40 miles from Michigan's U.P.

Posted: 10:22 a.m. Nov. 13, 2010

Infected buck found 40 miles from Michigan's U.P.

By Eric Sharp FREE PRESS STAFF WRITER

Comments (15) Recommend Print E-mail Letter to the editor Share Facebook Twitter FarkIt Digg Del.icio.us Reddit Newsvine Buzz up!A whitetail buck infected with chronic wasting disease has been found on a Wisconsin shooting preserve 40 miles from Michigan’s Upper Peninsula. That will trigger a ban on baiting and feeding deer in the UP, although the DNRE said it won’t affect the firearms deer season that opens Monday.

Mary Dettloff, a spokesperson the Department of Natural Resources and Environment, said that it’s too late to stop people from hunting over bait in the UP because so much corn, beets and other lures have already been put out. But the agency will ask hunters to stop putting out more.

Baiting already is banned in the Lower Peninsula, where a doe on a Kent County deer ranch was found to have the disease two years ago.

CWD is an invariably fatal disease of deer and elk that was first diagnosed in Colorado about 40 years ago. Wildlife biologists say that it is spread by deer coming in contact with mucous and urine from infected deer and that concentrating deer nose-to-nose at bait piles increases the chances of infection.

Dettloff said the DNRE was informed about the Wisconsin buck Friday but would not act on the discovery until it is confirmed by a “gold standard” test at an animal disease laboratory at Ames, Iowa (usually within a few weeks).

If it CWD is confirmed in the Ashland deer, the existing protocol the agency is required to ban baiting and recreational feeding of deer in the UP.

The protocol says, “In the event CWD is documented within Michigan or within 50 miles of Michigan’s border with another state or Canadian province, the (MDNRE) Director shall issue an interim order banning the use of bait and banning the feeding of deer and elk within the peninsula adjacent to the adjoining state or province with CWD or containing CWD.”

While baiting is banned in the Lower Peninsula, the law is very unpopular with many hunters and has been openly flouted. Corn, beets and carrots advertised as deer bait are stacked on pallets at stores and gas stations throughout the state, and bait dealers say hunters have been buying nearly as much as they did before the ban went into effect.

Contact ERIC SHARP: 313-222-2511 or esharp@freepress.com. Read more in his outdoors blog at freep.com/outdoorsblog. Order his book "Fishing Michigan" for $15.95 at www.freep.com/bookstore or by calling 800-245-5082.

Read more: Infected buck found 40 miles from Michigan's U.P. freep.com Detroit Free Press http://www.freep.com/article/20101113/SPORTS10/101113053/Infected-buck-found-40-miles-from-Michigan-s-U.P.#ixzz15Clw2t5t




http://www.freep.com/article/20101113/SPORTS10/101113053/Infected-buck-found-40-miles-from-Michigan-s-U-P-







CWD find raises threat up north Preliminary test shows ill deer at shooting preserve near Ashland By Paul A. Smith and Lee Bergquist of the Journal Sentinel

Nov. 12, 2010 (7) Comments

A white-tailed deer from a shooting preserve in northern Wisconsin has tested positive on a screening test for chronic wasting disease - a discovery that has the potential to bring the disease to a new part of the state.

Complicating the situation: An inspection of the fence at the 900-acre preserve in late October showed signs of damage, raising the possibility that deer could have escaped from the facility, a Department of Natural Resources official said Friday.

"The test and the fence issues certainly are a concern to the DNR," said Davin Lopez, chronic wasting disease coordinator for the agency.

The CWD-positive result was first identified in a test at the Wisconsin Veterinary Diagnostic Laboratory in Madison, according to the Wisconsin Department of Agriculture, Trade and Consumer Protection.

Tissue samples from the deer, reportedly a 3-year-old buck on a shooting preserve near Ashland in Bayfield County, have been sent to the Veterinary Diagnostic Laboratory in Ames, Iowa.

"We want to make sure it's not a false positive before making any formal announcements," said Lee Sensenbrenner, spokesman for the agriculture department.

The Ames lab at Iowa State University runs the "gold standard" test for CWD

Final results will not be known until Wednesday or later, said another agriculture spokeswoman, Donna Gilson.

Pending confirmation, the department declined to release the name of the shooting preserve.

If confirmed, the finding would be the first CWD-positive deer in northern Wisconsin. The fatal deer disease has been found in wild deer in a 1,000-square-mile Chronic Wasting Disease Management Zone in southern Wisconsin as well as game farms in other parts of the state. Two facilities in Portage County, one in Crawford County and another in Manitowoc County have had positive reports of CWD outside the state's disease management zone.

The disease was first discovered in Wisconsin in 2002.

"Not good," said Mike Riggle, a veterinarian, hunter and Wisconsin Conservation Congress member from Medford, of the latest development. "Everybody has been holding their breath for the last eight years."

"Folks in the north had thought that this isn't our problem," said Riggle, who also serves as chairman of the CWD Committee of the Wisconsin Conservation Congress. "Now, boom, it is our problem."

Riggle said the likelihood of a false-positive was "very, very remote."

The buck was tested as part of a protocol on deer farms in the state. The state agriculture department has authority over deer farms in Wisconsin.

The DNR has begun contingency planning, said Tom Hauge, wildlife chief, including possibly increased testing of wild deer in the area.

Deer shot in the area during this year's hunting season will be tested for the disease.

Previous testing of over 1,000 wild deer in the Ashland area had turned up no CWD-positives, according to the DNR.

Though fatal to deer and elk, CWD has shown no link to human health or livestock.

Also, a positive test doesn't necessarily expose wild deer in the area to the disease.

A game farm near Almond in Portage County produced 82 infected deer. Most were killed in 2006, and the rash of positives represented the highest infection rate ever reported in the United States, the DNR said.

Before the shooting, officials discovered that a hole had been cut in the fence and that the captive bucks - about 30 - had escaped and were never found.

But state records show that analyses of 2,559 wild deer from Portage and Waushara counties have shown no signs of the disease.



http://www.jsonline.com/news/wisconsin/107561383.html



CWD, GAME FARMS, BAITING, AND POLITICS

http://chronic-wasting-disease.blogspot.com/2009/01/cwd-game-farms-baiting-and-politics.html





ALSO, NOTE MINERAL LICKS A POSSIBLE SOURCE AND TRANSMISSION MODE FOR CWD ;


http://chronic-wasting-disease.blogspot.com/2009/08/third-international-cwd-symposium-july.html



http://www.cwd-info.org/pdf/3rd_CWD_Symposium_utah.pdf




Friday, February 20, 2009

Both Sides of the Fence: A Strategic Review of Chronic Wasting Disease


http://chronic-wasting-disease.blogspot.com/2009/02/both-sides-of-fence-strategic-review-of.html




Saturday, September 06, 2008

Chronic wasting disease in a Wisconsin white-tailed deer farm 79% INFECTION RATE

Contents: September 1 2008, Volume 20, Issue 5

snip...see full text ;


http://chronic-wasting-disease.blogspot.com/2008/11/commentary-crimes-hurt-essence-of.html




Tuesday, February 09, 2010

Chronic Wasting Disease: Surveillance Update North America: February 2010

***


>>> In addition, we documented horizontal transmission of CWD from inoculated mice and to un-inoculated cohabitant cage-mates. <<< http://ajp.amjpathol.org/cgi/content/abstract/ajpath.2010.090710v1




disturbing. ...TSS


http://chronic-wasting-disease.blogspot.com/2010/02/chronic-wasting-disease-surveillance.html



Sunday, December 06, 2009

Detection of Sub-Clinical CWD Infection in Conventional Test-Negative Deer Long after Oral Exposure to Urine and Feces from CWD+ Deer

http://chronic-wasting-disease.blogspot.com/2009/12/detection-of-sub-clinical-cwd-infection.html



Wednesday, March 18, 2009

Detection of CWD Prions in Urine and Saliva of Deer by Transgenic Mouse Bioassay

http://chronic-wasting-disease.blogspot.com/2009/03/detection-of-cwd-prions-in-urine-and.html



Tuesday, June 16, 2009

Infectious Prions in Pre-Clinical Deer and Transmission of Chronic Wasting Disease Solely by Environmental Exposure

http://chronic-wasting-disease.blogspot.com/2009/06/infectious-prions-in-pre-clinical-deer.html



Wednesday, October 14, 2009

Detection of protease-resistant cervid prion protein in water from a CWD-endemic area

http://chronic-wasting-disease.blogspot.com/2009/10/detection-of-protease-resistant-cervid.html



AS THE CROW FLIES, SO DOES CWD

Sunday, November 01, 2009

American crows (Corvus brachyrhynchos) and potential spreading of CWD through feces of digested infectious carcases

http://chronic-wasting-disease.blogspot.com/2009/11/american-crows-corvus-brachyrhynchos.html



Wednesday, January 07, 2009

CWD to tighten taxidermy rules Hunters need to understand regulations

http://chronic-wasting-disease.blogspot.com/2009/01/cwd-to-tighten-taxidermy-rules-hunters.html




Wednesday, September 08, 2010



CWD PRION CONGRESS SEPTEMBER 8-11 2010



http://chronic-wasting-disease.blogspot.com/2010/09/cwd-prion-2010.html





P35

ADAPTATION OF CHRONIC WASTING DISEASE (CWD) INTO HAMSTERS, EVIDENCE OF A WISCONSIN STRAIN OF CWD

Chad Johnson1, Judd Aiken2,3,4 and Debbie McKenzie4,5 1 Department of Comparative Biosciences, University of Wisconsin, Madison WI, USA 53706 2 Department of Agriculture, Food and Nutritional Sciences, 3 Alberta Veterinary Research Institute, 4.Center for Prions and Protein Folding Diseases, 5 Department of Biological Sciences, University of Alberta, Edmonton AB, Canada T6G 2P5 The identification and characterization of prion strains is increasingly important for the diagnosis and biological definition of these infectious pathogens. Although well-established in scrapie and, more recently, in BSE, comparatively little is known about the possibility of prion strains in chronic wasting disease (CWD), a disease affecting free ranging and captive cervids, primarily in North America. We have identified prion protein variants in the white-tailed deer population and demonstrated that Prnp genotype affects the susceptibility/disease progression of white-tailed deer to CWD agent. The existence of cervid prion protein variants raises the likelihood of distinct CWD strains. Small rodent models are a useful means of identifying prion strains. We intracerebrally inoculated hamsters with brain homogenates and phosphotungstate concentrated preparations from CWD positive hunter-harvested (Wisconsin CWD endemic area) and experimentally infected deer of known Prnp genotypes. These transmission studies resulted in clinical presentation in primary passage of concentrated CWD prions. Subclinical infection was established with the other primary passages based on the detection of PrPCWD in the brains of hamsters and the successful disease transmission upon second passage. Second and third passage data, when compared to transmission studies using different CWD inocula (Raymond et al., 2007) indicate that the CWD agent present in the Wisconsin white-tailed deer population is different than the strain(s) present in elk, mule-deer and white-tailed deer from the western United States endemic region.


http://www.istitutoveneto.it/prion_09/Abstracts_09.pdf




Potential Venison Exposure Among FoodNet Population Survey Respondents, 2006-2007

Ryan A. Maddox1*, Joseph Y. Abrams1, Robert C. Holman1, Lawrence B. Schonberger1, Ermias D. Belay1 Division of Viral and Rickettsial Diseases, National Center for Zoonotic, Vector-Borne, and Enteric Diseases, Centers for Disease Control and Prevention, Atlanta, GA *Corresponding author e-mail: rmaddox@cdc.gov

The foodborne transmission of bovine spongiform encephalopathy to humans, resulting in variant Creutzfeldt-Jakob disease, indicates that humans can be susceptible to animal prion diseases. However, it is not known whether foodborne exposure to the agent causing chronic wasting disease (CWD) in cervids can cause human disease. The United States Foodborne Diseases Active Surveillance Network (FoodNet) conducts surveillance for foodborne diseases through an extensive survey administered to respondents in selected states. To describe the frequency of deer and elk hunting and venison consumption, five questions were included in the 2006-2007 FoodNet survey. This survey included 17,372 respondents in ten states: California, Colorado, Connecticut, Georgia, Maryland, Minnesota, New Mexico, New York, Oregon, and Tennessee. Of these respondents, 3,220 (18.5%) reported ever hunting deer or elk, with 217 (1.3%) reporting hunting in a CWD-endemic area (northeastern Colorado, southeastern Wyoming, and southwestern Nebraska). Of the 217 CWD-endemic area hunters, 74 (34.1%) were residents of Colorado. Respondents reporting hunting were significantly more likely to be male than female (prevalence ratio: 3.3, 95% confidence interval: 3.1-3.6) and, in general, older respondents were significantly more likely to report hunting than younger respondents. Venison consumption was reported by more than half (67.4%) of the study population, and most venison consumers (94.1%) reported that at least half of their venison came from the wild. However, more than half (59.1%) of the consumers reported eating venison only one to five times in their life or only once or twice a year. These findings indicate that a high percentage of the United States population engages in hunting and/or venison consumption. If CWD continues to spread to more areas across the country, a substantial number of people could potentially be exposed to the infectious agent.

http://www.cwd-info.org/pdf/3rd_CWD_Symposium_utah.pdf




Sunday, April 12, 2009

CWD UPDATE Infection Studies in Two Species of Non-Human Primates and one Environmental reservoir infectivity study and evidence of two strains

http://chronic-wasting-disease.blogspot.com/2009/04/cwd-update-infection-studies-in-two.html




I will quote what one of the leading scientist in the world on prion disease once said about CWD, and then post some data on this topic. Good question, one that should be addressed. I will attempt to address it. I am a meat eater, and I don't care what you and others eat, but on the topic of human and animal Transmissible Spongiform Encephalopathy, I can assure you that you have not been told the complete truth. This is a long post, take the information, and please look at the source of the data. I post this data on blogs, no advertisements, not making money doing this. The information is for your benefit, please use as you wish. ...kind regards, terry

A. Aguzzi - Chronic Wasting Disease (CWD) also needs to be addressed.

Most serious because of rapid horizontal spread and higher prevalence than BSE in UK, up to 15% in some populations.

Also may be a risk to humans - evidence that it is not dangerous to humans is thin. ...end

REMEMBER, there are over twenty strains of typical scrapie, and the atypical scrapie cases (Nor-98) are mounting, two documented strains of Transmissible Mink Encephalopathy, and 3 strains of BSE in cattle, all of which have been documented in North America, all have been shown to transmit to man via lab studies in mice, with the L-type atypical BSE being much more virulent. Also, now there are two strains of CWD. all these TSE in different animals have been rendered and put into feed for livestock producing animals for human and animal in the USA. This is fact.

can humans get a prion disease from deer or elk that have CWD ?

as someone else stated here, no one knows for sure to date, but the likelyhood of being exposed to CWD from eating a CWD deer or elk is high, and then years on down the road, regardless whether or not this person ever goes clinical, due to any medical surgical, or dental procedures, blood donations, the agent will continue to spread, more humans exposed. the fact that some of these atypical TSE are mutating and becoming more virulent is very troublesome. the incubation time is shortened.

I assure you that the FDA did not recall this CWD postive elk meat in commerce, for the well being of the dead CWD postive elk ;

Wednesday, March 18, 2009

Noah's Ark Holding, LLC, Dawson, MN RECALL Elk products contain meat derived from an elk confirmed to have CWD NV, CA, TX, CO, NY, UT, FL, OK RECALLS AND FIELD CORRECTIONS: FOODS CLASS II

please see ;

RECALLS AND FIELD CORRECTIONS: FOODS CLASS II

___________________________________

PRODUCT a) Elk Meat, Elk Tenderloin, Frozen in plastic vacuum packaging. Each package is approximately 2 lbs., and each case is approximately 16 lbs.; Item number 755125, Recall # F-129-9;

b) Elk Meat, Elk Trim, Frozen; Item number 755155, Recall # F-130-9;

c) Elk Meat, French Rack, Chilled. Item number 755132, Recall # F-131-9;

d) Elk Meat, Nude Denver Leg. Item number 755122, Recall # F-132-9;

e) Elk Meat, New York Strip Steak, Chilled. Item number 755128, Recall # F-133-9;

f) Elk Meat, Flank Steak Frozen. Item number 755131, Recall # F-134-9; CODE Elk Meats with production dates of December 29, 30, and 31 RECALLING FIRM/MANUFACTURER Recalling Firm: Sierra Meats, Reno, NV, by telephone on January 29, 2009 and press release on February 9, 2009. Manufacturer: Noah’s Ark Holding, LLC, Dawson, MN. Firm initiated recall is ongoing. REASON Elk products contain meat derived from an elk confirmed to have Chronic Wasting Disease (CWD). VOLUME OF PRODUCT IN COMMERCE Unknown DISTRIBUTION NV, CA, TX, CO, NY, UT, FL, OK

___________________________________

END OF ENFORCEMENT REPORT FOR March 18, 2009

###

http://www.fda.gov/Safety/Recalls/EnforcementReports/ucm154840.htm


http://chronic-wasting-disease.blogspot.com/2009/03/noahs-ark-holding-llc-dawson-mn-recall.html


http://chronic-wasting-disease.blogspot.com/2009/02/exotic-meats-usa-announces-urgent.html


Sunday, April 12, 2009

CWD UPDATE Infection Studies in Two Species of Non-Human Primates and one Environmental reservoir infectivity study and evidence of two strains

http://chronic-wasting-disease.blogspot.com/2009/04/cwd-update-infection-studies-in-two.html


Thursday, April 03, 2008

A prion disease of cervids: Chronic wasting disease

2008 1: Vet Res. 2008 Apr 3;39(4):41

A prion disease of cervids: Chronic wasting disease

Sigurdson CJ.

snip...

*** twenty-seven CJD patients who regularly consumed venison were reported to the Surveillance Center***,

snip...

full text ;

http://chronic-wasting-disease.blogspot.com/2008/04/prion-disease-of-cervids-chronic.html


From: TSS (216-119-163-189.ipset45.wt.net)

Subject: CWD aka MAD DEER/ELK TO HUMANS ???

Date: September 30, 2002 at 7:06 am PST

From: "Belay, Ermias"

To:

Cc: "Race, Richard (NIH)" ; ; "Belay,

Ermias"

Sent: Monday, September 30, 2002 9:22 AM

Subject: RE: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS

Dear Sir/Madam,

In the Archives of Neurology you quoted (the abstract of which was

attached to your email), we did not say CWD in humans will present like

variant CJD.

That assumption would be wrong. I encourage you to read the whole

article and call me if you have questions or need more clarification

(phone: 404-639-3091). Also, we do not claim that "no-one has ever been

infected with prion disease from eating venison." Our conclusion stating

that we found no strong evidence of CWD transmission to humans in the

article you quoted or in any other forum is limited to the patients we

investigated.

Ermias Belay, M.D.

Centers for Disease Control and Prevention


-----Original Message-----

From:

Sent: Sunday, September 29, 2002 10:15 AM

To: rr26k@nih.gov; rrace@niaid.nih.gov; ebb8@CDC.GOV

Subject: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG

HUNTERS

Sunday, November 10, 2002 6:26 PM ......snip........end..............TSS

SEE also ;

A. Aguzzi - Chronic Wasting Disease (CWD) also needs to be addressed. Most

serious because of rapid horizontal spread and higher prevalence than BSE in

UK, up to 15% in some populations. Also may be a risk to humans - evidence

that it is not dangerous to humans is thin.

http://www.tseandfoodsafety.org/activities/bse_conference_basel_april_02/2summar


SNIP...END...TSS

Chronic Wasting Disease and Potential Transmission to Humans

Ermias D. Belay,* Ryan A. Maddox,* Elizabeth S. Williams,? Michael W. Miller,? Pierluigi Gambetti,§ and Lawrence B. Schonberger*

*Centers for Disease Control and Prevention, Atlanta, Georgia, USA; ?University of Wyoming, Laramie, Wyoming, USA; ?Colorado Division of Wildlife, Fort Collins, Colorado, USA; and §Case Western Reserve University, Cleveland, Ohio, USA

Suggested citation for this article: Belay ED, Maddox RA, Williams ES, Miller MW, Gambetti P, Schonberger LB. Chronic wasting disease and potential transmission to humans. Emerg Infect Dis [serial on the Internet]. 2004 Jun [date cited]. Available from:

http://www.cdc.gov/ncidod/EID/vol10no6/03-1082.htm


----------------------------------------------------------


Chronic wasting disease (CWD) of deer and elk is endemic in a tri-corner area of Colorado, Wyoming, and Nebraska, and new foci of CWD have been detected in other parts of the United States. Although detection in some areas may be related to increased surveillance, introduction of CWD due to translocation or natural migration of animals may account for some new foci of infection. Increasing spread of CWD has raised concerns about the potential for increasing human exposure to the CWD agent. The foodborne transmission of bovine spongiform encephalopathy to humans indicates that the species barrier may not completely protect humans from animal prion diseases. Conversion of human prion protein by CWD-associated prions has been demonstrated in an in vitro cell-free experiment, but limited investigations have not identified strong evidence for CWD transmission to humans. More epidemiologic and laboratory studies are needed to monitor the possibility of such transmissions.

snip...full text ;

http://www.cdc.gov/ncidod/EID/vol10no6/03-1082.htm


Volume 12, Number 10-October 2006

Research

Human Prion Disease and Relative Risk Associated with Chronic Wasting Disease

Samantha MaWhinney,* W. John Pape,? Jeri E. Forster,* C. Alan Anderson,?§ Patrick Bosque,?¶ and Michael W. Miller#

*University of Colorado at Denver and Health Sciences Center, Denver, Colorado, USA; ?Colorado Department of Public Health and Environment, Denver, Colorado, USA; ?University of Colorado School of Medicine, Denver, Colorado, USA; §Denver Veteran's Affairs Medical Center, Denver, Colorado, USA; ¶Denver Health Medical Center, Denver, Colorado, USA; and #Colorado Division of Wildlife, Fort Collins, Colorado, USA

Suggested citation for this article

The transmission of the prion disease bovine spongiform encephalopathy (BSE) to humans raises concern about chronic wasting disease (CWD), a prion disease of deer and elk. In 7 Colorado counties with high CWD prevalence, 75% of state hunting licenses are issued locally, which suggests that residents consume most regionally harvested game. We used Colorado death certificate data from 1979 through 2001 to evaluate rates of death from the human prion disease Creutzfeldt-Jakob disease (CJD). The relative risk (RR) of CJD for CWD-endemic county residents was not significantly increased (RR 0.81, 95% confidence interval [CI] 0.40-1.63), and the rate of CJD did not increase over time (5-year RR 0.92, 95% CI 0.73-1.16). In Colorado, human prion disease resulting from CWD exposure is rare or nonexistent. However, given uncertainties about the incubation period, exposure, and clinical presentation, the possibility that the CWD agent might cause human disease cannot be eliminated.

snip... full text ;

http://0-www.cdc.gov.mill1.sjlibrary.org/ncidod/EID/vol12no10/06-0019.htm


full text ;


http://chronic-wasting-disease.blogspot.com/2006_12_01_archive.html



(10) Transmission of Elk and Deer Prions to Transgenic Mice

http://jvi.asm.org/cgi/content/abstract/80/18/9104


(30) Neurobiology of Disease Chronic Wasting Disease of Elk: Transmissibility to Humans Examined by Transgenic Mouse Models

http://www.jneurosci.org/cgi/content/short/25/35/7944


(13) Prions in Skeletal Muscles of Deer with Chronic Wasting Disease

http://www.sciencemag.org/cgi/content/abstract/sci;311/5764/1117


(14) Volume 15, Number 5–May 2009 Research Chronic Wasting Disease Prions in Elk Antler Velvet

http://www.cdc.gov/eid/content/15/5/696.htm


Friday, May 14, 2010

Prion Strain Mutation Determined by Prion Protein Conformational Compatibility and Primary Structure

Published Online May 13, 2010 Science DOI: 10.1126/science.1187107 Science Express Index

http://chronic-wasting-disease.blogspot.com/2010/05/prion-strain-mutation-determined-by.html



In Confidence - Perceptions of unconventional slow virus diseases of animals in the USA - APRIL-MAY 1989 - G A H Wells

3. Prof. A Robertson gave a brief account of BSE. The US approach was to accord it a very low profile indeed. Dr. A Thiermann showed the picture in the ''Independent'' with cattle being incinerated and thought this was a fanatical incident to be avoided in the US at all costs. BSE was not reported in the USA.

snip...

CWD occurred principally in two locations, this one at Sybille and in a similar faccility at Fort Collins, Colorado, some 120 miles southwest. It was estimated that in total probably 60-70 cases of CWD have occurred.

It was difficult to gain a clear account of incidence and temporal sequence of events (-this presumably is data awaiting publication - see below) but during the period 1981-1984, 10-15 cases occurred at the Sybille facility.

The moribidity amongst mule deer in the facilities ie. those of the natural potentially exposed group has been about 90% with 100% mortality.

snip...

Spraker suggested an interesting explanation for the occurrence of CWD. The deer pens at the Foot Hills Campus were built some 30-40 years ago by a Dr. Bob Davis. At or abut that time, allegedly, some scrapie work was conducted at this site. When deer were introduced to the pens they occupied ground that had previously been occupied by sheep.

see full text 33 pages ;


http://collections.europarchive.org/tna/20080102193705/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf



CHRONIC WASTING DISEASE BLOG



http://chronic-wasting-disease.blogspot.com/



TSS


UPDATE !!! FALSE POSITIVE ???


Published November 19 2010 Wisconsin DNR to continue CWD testing The Wisconsin DNR made plans to take deer tissue samples this weekend after a screening test showed a possible case of chronic wasting disease at a game farm near Ashland. Even though that test turned out to be a false positive, the DNR will go ahead and take samples from hunter-killed and car-killed deer within a 10-mile radius of Ashland.


The Wisconsin DNR made plans to take deer tissue samples this weekend after a screening test showed a possible case of chronic wasting disease at a game farm near Ashland. Even though that test turned out to be a false positive, the DNR will go ahead and take samples from hunter-killed and car-killed deer within a 10-mile radius of Ashland.

Hunters supplying samples for testing will be able to track results at www.dnr.wi.gov. Test results will take three to four weeks to be posted.

Here is a list of sampling stations where hunters can take deer for disease testing Saturday and Sunday:

•Anglers All, 2803 Lakeshore Drive E., Ashland

•Pearce’s Sausage Kitchen, 61327 Dahlstrom Road, Ashland

•Woody’s Taxidermy, 1109 Vaughn Ave., Ashland

•Bayside Taxidermy, 1110 Lakeshore Drive, Ashland

•Chequamegon Taxidermy, 73740 Strecker Road, Washburn

•Brian Weber Processing, 29125 State Highway 137, Ashland

•Ino Bar, 19020 U.S. Highway 2, Ino

•Washburn Holiday Station, 606 W. Bayfield St., Washburn




http://www.duluthnewstribune.com/event/article/id/184347/group/Sports/




The Wisconsin Veterinary Diagnostic Lab - WVDL - involved in controversy over interpreting CWD test results and public disclosure.

An article on Wisconsin CWD test results by Associated Press reporter, Robert Imrie, has brought to light concerns over test procedures, test accuracy, and the reliability of test information released to hunters and the general public. The controversy surrounds 117 deer that initially tested positive on the new IDEXX rapid-screening test put into place by the DNR for the 2003 season. Because the older IHC test did not confirm those positive results, the protocol followed by the agency and its testing lab (WVDL) determined that the IDEXX test results were false. In fact, 74% of the IDEXX positives were eventually determined to be false - only 26% were confirmed by the older test. This low correlation between the two tests flies in the face of the results of the USDA trials of the test that showed almost 100% agreement between the two tests. Without a high correlation between the new IDEXX test and the older IHC test, the IDEXX would not have been certified for use.

Among the sources contacted in the Imrie investigation were some leaders in a DNR watchdog group called CALFARR (Citizens and Landowners for a Rational Response) who have long opposed the extreme response by the agency to the discovery of CWD in southern Wisconsin. The group has been conducting their own investigation into reporting failures and inconsistencies. On March 9th, they lodged a formal appeal with State Senate leader Erpenbach claiming a "hunters right to know" ALL of the results of the screening tests - not just those the DNR chose's to release. CALFARR believes that hunters who voluntarily submit samples for testing are entitled to full disclosure of test results - not a filtered version.

The IDEXX test only screens for CWD Suspects? The DNR and its Lab - the Wisconsin Veterinary Diagnostic Lab - are arguing that the IDEXX test only produces a "suspect" result and thus it would be misleading or confusing to report such results to hunters.

What is odd about this position is that IDEXX itself makes quite strong representations of the accuracy of its CWD test. Its web site reports that the "proven IDEXX ELISA" CWD test is extremely accurate: " . . . 98.8% sensitivity and 100% specificity (sensitivity validated through IHC confirmation testing)."

IDEXX Laboratories claims on their website that every deer from data sets used in IDEXX test validation with an absorbance value over .21 has also tested positive using IHC testing. This represents a specificity of 100%. The confirmation testing data the company used to gain USDA certification are on file with the firm. Positive and negative controls are provided in each test. Positive controls demonstrate the presence of CWD and react to give IDEXX values >0.40, and negative controls demonstrate the absence of CWD and give IDEXX values less than 0.15.

IDEXX ELISA technology could offer far greater sensitivity and reliability than the older IHC methods. The older IHC method suffers from potential sampling error plus it involves human subjectivity in interpreting the results. In IHC, a paper thin slice is taken from the tissue for microscopic examination. There is always a possibility that the paper thin slice fails to capture deformed CWD prions that may be present in the larger homogenized tissue sample used for IDEXX testing. Several sections must be taken through various areas of the same tissue used for ELISA in order for IHC to be accurate. If the error doesn't occur at this sampling stage, it may occur in the reading of the slide. While science based, this reading is an art form that depends greatly upon the technician's experience and intellectual discipline. As in radiology, two Radiologists may disagree on the interpretation of an x-ray film.

ELISA technology on the other hand - uses a larger tissue sample and homogenizes it. Thus it involves a more representative sample of the larger piece of tissue. The equipment provides a digital readout allowing no room for subjectivity or individual differences in technician experience or competence. A reading of .41 will be what it is no matter who reads it.

Public records from the WVDL of IDEXX test result data showed 26 deer deemed "negative" for CWD by the Lab & the DNR had IDEXX results were more than twice the IDEXX CWD positive threshold! And 5 of these "negative" confirmations exceeded the IDEXX positive optical density threshold by a factor 5! (the positive threshold is an optical density reading of .21 . . . 5 of the rejected samples had densities exceeding 1.05).

So considering the ELISA design of the IDEXX test should reduce subjectivity and other sources of error, if a reading of 1.05 - 5 times the "suspect" threshold - turns out to be negative, wouldn't that cause a reasonable person to suspect something isn't working properly? Is the basic test is badly flawed in its construction or were gross errors were made by the technician? And if such a large discrepancy occurs - not just once - but five times, isn't something clearly amuck?

It would seem that unless the WVDL discovers and admits the possibility of technician error, it must consider that the IDEXX test itself may be unreliable. We know that the record of testing in Colorado using a similar ELISA test kit by an IDEXX competitor, Bio-Rad, has a near-spotless record of confirmatory testing (only 4 times in 47,000 cases did the Bio-Rad ELISA test and the IHC test fail to agree).

How Golden is the Gold Standard? The DNR and the WVDL often refer to the older IHC test as the Gold Standard - a test whose accuracy and reliability is beyond question. Thus we were surprised when reading a Colorado State CWD Surveillance study to come upon the following statement:

"Most reference tests used in validation studies are imperfect and are incorrectly termed “gold standards”. Many authors have shown that the use of these imperfect reference tests for the calculation of sensitivity and specificity of new tests result in estimates that are biased (Staquet et al., 1981; Enoe et al., 2000). In the simple case, where the reference test is imperfectly sensitive but perfectly specific (e.g., bacterial, viral, or parasite isolation), the sensitivity and specificity of the new test will likely both be underestimated."

This same study report also explains the difficulty in properly interpreting IHC results:

" . . . The IHC is time consuming and requires specialized technical skills. Furthermore, IHC interpretation is subjective and can be influenced by prior knowledge of the case and associated results from the screening tests. Several new rapid screening tests are being validated to complement available techniques for the purpose of large scale screening for these diseases. Some of these tests have been validated and are currently being applied in disease control programs in several countries. Other tests are currently being validated for both screening and confirmation of these diseases.

All of these tests require the collection of appropriate clinical specimens, mainly the appropriate obex site of brain tissue, or the region proximal to the cortex in lymph nodes. Selection of the appropriate clinical specimens (tissue type, amount of tissue collected, etc) is an essential component if these tests are to have good diagnostic accuracy. Furthermore, it is known that the prion agent of these diseases tends to be unevenly distributed in the tissue specimens."

What is your testing objective? Our internet research on this subject found an interesting a course outline on VETERINARY EPIDEMIOLOGY (Caution - long download time) that discussed, among other matters, how research objectives determine the type of procedures used. In employing a two test protocol, the lab may chose to run the tests parallel to one another or in series:

"Parallel interpretation With parallel test interpretation, an animal is considered to have the disease, if one or more tests are positive. This means the animal is being asked to ‘prove’ that it is healthy.

Series interpretation With serial test interpretation, the animal is considered to have the disease if all tests are positive. In other words, the animal is being asked to ‘prove’ that it has the condition."

From this it seems clear our Wisconsin officials are following a "series interpretation" strategy - thus the animal must test positive in both tests and "prove" it has the condition. It is not being asked to "prove" it is healthy. Thus our procedure means we can be very, very confident that every case we deem CWD positive is "in fact" CWD positive. We want to be quite sure we have no false positives.

On the other hand our procedure allows room for the possibility that some CWD negatives are "in fact" CWD positives. This is the direct result of our testing objective aiming to insure against false positives.

Thus we have a conflict of testing objectives. The DNR wants to be absolutely sure that when a deer is pronounced CWD positive, it is in fact CWD positive. Hunters - who request tests - want to know that when their deer is pronounced CWD negative, it is in fact CWD negative!

Another example of the needs of the Agency bureaucracy taking priority over the needs of hunters.

--Ross Reinhold, April 13, 2004 & April 29, 2004 roscoe@mhtc.net

Some information for this


http://www.caids-wi.org/IDEXX_cwd2.html



http://wildlife.state.co.us/NR/rdonlyres/8A40833F-5DC5-46FD-9A0F-36EF32582F67/0/Field_Valid.pdf




PLEASE BE ADVISED, test for prions in different species is still not an exact science, especially in most cases where to look NOT to find, as with the case of BSE in USA cattle. ...TSS



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




BIO-RAD

-------- Original Message --------
Subject: USA BIO-RADs INCONCLUSIVEs
Date: Fri, 17 Dec 2004 15:37:28 -0600
From: "Terry S. Singeltary Sr." To: susan_berg@bio-rad.com

Hello Susan and Bio-Rad,

Happy Holidays!

I wish to ask a question about Bio-Rad and USDA BSE/TSE testing and there inconclusive. IS the Bio-Rad test for BSE/TSE that complicated, or is there most likely some human error we are seeing here?

HOW can Japan have 2 positive cows with No clinical signs WB+, IHC-, HP- , BUT in the USA, these cows are considered 'negative'?

IS there more politics working here than science in the USA?

What am I missing?

-------- Original Message --------
Subject: Re: USDA: More mad cow testing will demonstrate beef's safety
Date: Fri, 17 Dec 2004 09:26:19 -0600
From: "Terry S. Singeltary Sr." snip...end

Experts doubt USDA's mad cow results

snip...END

WELL, someone did call me from Bio-Rad about this, however it was not Susan Berg. but i had to just about take a blood oath not to reveal there name. IN fact they did not want me to even mention this, but i feel it is much much to important. I have omitted any I.D. of this person, but thought I must document this ;

Bio-Rad, TSS phone conversation 12/28/04

Finally spoke with ;

Bio-Rad Laboratories 2000 Alfred Nobel Drive Hercules, CA 94547 Ph: 510-741-6720 Fax: 510-741-5630 Email: XXXXXXXXXXXXXXXXXX

at approx. 14:00 hours 12/28/04, I had a very pleasant phone conversation with XXXX XXXXX about the USDA and the inconclusive BSE testing problems they seem to keep having. X was very very cautious as to speak directly about USDA and it's policy of not using WB. X was very concerned as a Bio-Rad official of retaliation of some sort. X would only speak of what other countries do, and that i should take that as an answer. I told X I understood that it was a very loaded question and X agreed several times over and even said a political one.

my question;

Does Bio-Rad believe USDA's final determination of False positive, without WB, and considering the new atypical TSEs not showing positive with -IHC and -HP ???

ask if i was a reporter. i said no, i was with CJD Watch and that i had lost my mother to hvCJD. X did not want any of this recorded or repeated.

again, very nervous, will not answer directly about USDA for fear of retaliation, but again said X tell me what other countries are doing and finding, and that i should take it from there. "very difficult to answer"

"very political"

"very loaded question"

outside USA and Canada, they use many different confirmatory tech. in house WB, SAF, along with IHC, HP, several times etc. you should see at several talks meetings (TSE) of late Paris Dec 2, that IHC- DOES NOT MEAN IT IS NEGATIVE. again, look what the rest of the world is doing. said something about Dr. Houston stating; any screening assay, always a chance for human error. but with so many errors (i am assuming X meant inconclusive), why are there no investigations, just false positives? said something about ''just look at the sheep that tested IHC- but were positive''. ...

TSS

-------- Original Message --------
Subject: Your questions
Date: Mon, 27 Dec 2004 15:58:11 -0800
From: To: flounder@wt.net

Hi Terry:

............................................snip

Let me know your phone number so I can talk to you about the Bio-Rad BSE test. Thank you

Regards

Bio-Rad Laboratories 2000 Alfred Nobel Drive Hercules, CA 94547 Ph: 510-741-6720 Fax: 510-741-5630 Email:

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

END...TSS

######### https://listserv.kaliv.uni-karlsruhe.de/warc/bse-l.html ##########


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


END....TSS

-------- Original Message --------
Subject: RE: Greetings again Professor Aguzzi ... TSS
Date: Fri, 11 Mar 2005 09:19:49 +0100
From: "Adriano Aguzzi" T
o: "'Terry S. Singeltary Sr.'"

Dear Mr. Singeltary

I sympathize with your wish to have the most sensitive assay implemented. However, the situation is not as simple as one might think. In the case of homogeneously distributed agent, biochemical detection of PrPSc is indeed likely to be more sensitive than immunohistochemistry. In the case of variegated, punctate distribution of the agent, morphological methods may indeed be an asset.

There are also issues of feasibility. In my laboratory, we routinely run phosphotungstic acid precipitation followed by Western blotting. However, this is an extraordinarily cumbersome procedure. The sensitivity is increased vastly, but the amount of work needed is also amazing. There is no way I could see our own procedure implemented for mass screening of millions of cows - unless one would draft a veritable army of laboratory technicians.

For all these reasons, while I see all your points, I feel unable to offer a strong public opinion in favor or against any specific methods. The final decision needs to take into account a variety of complex factors, and that is why I believe that it is best left to a panel of experts rather than to a public discussion.

Best regards Adriano Aguzzi

____________________________

Prof. Adriano Aguzzi (MD PhD hc FRCP FRCPath) Institute of Neuropathology, University Hospital of Zürich Schmelzbergstrasse 12, CH-8091 Zürich, Switzerland Tel. ++41-1-255 2107 Tel. (direct line): 2869 Fax: ++41-1-255 4402, cellular: +41-79-320 1516 http://www.unizh.ch/pathol/neuropathologie/

-----Original Message-----
From: Terry S. Singeltary Sr. [mailto:flounder@wt.net]
Sent: Thursday, March 10, 2005 20:18
To: adriano@pathol.unizh.ch
Subject: Greetings again Professor Aguzzi ... TSS

Greetings again Professor Aguzzi,

A kind greetings from Texas. I hope you do not mind, but I must ask you several questions that will put you in the hot seat. Someone with credibility must come forward, such as yourself and speak out about the fact of the non scientific approach that USDA et al has take after the first diagnosis of BSE in the USA. This being, the refusal to use Western Blot on any suspicious or inconclusive BSE/TSE test. IHC is like a brain biopsy on trying to diagnose a CJD case. IF you take the sample from a part of the brain that is not that tainted, you will not get a reading. WB is much more sensitive, especially now with the Phospohtugstic acid precipitation step. IF Prusiners CDI was validated, who knows, that might even be more sensitive. Bottom line, we need you to come forward and state publicly ''the facts'' about USDA et al decision not to use WB on not only questionable samples, but on ALL samples. would you be willing to comment on this, to me or someone from the media (under the understanding it will be for the public)? I have several questions for you??? This is very very important in terms of human health (i.e. that nov. pos. pos. incl. neg cow).

P.S. there is one other top TSE scientist that has come forward and said what the USDA et al did with that cow was ''not logical''. (this will not be published for another 3 or 4 weeks). ONE other TOP TSE scientist saying the same thing would be much better for the public to hear and understand. anyway, does not hurt to ask, and i hope you come through here for us. I know this is a very loaded question, but times a wasting, and human health is at risk here...

thank you, with kindest regards,

I am sincerely,

Terry S. Singeltary Sr.

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

I would like to add to the first paragraph of Adriano Aguzzis comments. We have seen cases in Europe, where a positive result obtained with our Western blot rapid test(Prionics-Check WESTERN)could not be confirmed with IHC, but with the OIE-Western blot procedure, and we have also seen cases where the result could be confirmed by IHC but not by OIE-Western blot. As Adrino Aguzzi pointed out both IHC and OIE-Western have their limitations, but when combined and when performed well they pick up BSE reliably. In case of doubt, i.e. if a rapid test comes out consistently positive but an initial attempt of confirmation with IHC (or OIE-Western) fails, we recommend to routinely do a second test with the respective alternative method. This is the procedure most national reference centers, which are responsible for final confirmation of BSE cases, are following. Regards Markus Moser Prionics

-------- Original Message --------
Subject: Q&A Dr. Jean-Philippe Deslys USDA REFUSAL TO USE WB ON TEXAS COW WITH BSE SYMPTOMS (FULL TEXT)
Date: Fri, 22 Apr 2005 11:53:47 -0500
From: "Terry S. Singeltary Sr." Reply-To: Bovine Spongiform Encephalopathy
To: BSE-L@LISTS.UNI-KARLSRUHE.DE

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

Q&A Dr. Jean-Philippe Deslys

1. What is the standard regime for testing of suspect animals in the EU?

The regime is an initial screening by a high-output test, the Bio-Rad test. If a result raises suspicion, a confirmatory test is conducted with the Western blot test.

2. How long has this been the case?

It s a fairly recent development. Only recently has the Western blot test become sensitive enough, with the addition of phospohtungstic acid precipitation step. The Bio-Rad test (which Deslys helped develop) is extremely sensitive, and the standard Western blot is extremely reliable with high-signal test results. However, it had to be made more sensitive for low-signal (samples with low density of malformed prions) samples. It has been made more sensitive.

Reproducibility is the problem with the IHC test. It is not standardized; depending on the lab and its protocols, or even on the technician involved in the test, one can get conflicting results.

3. Is there a way to measure the three tests in sensitivity, accuracy and objectivity?

Historically, yes. The IHC was the gold standard at one point, but we have shifted to the Western blot. It requires less work, it is more sensitive and its results are reproducible. IHC relies on localization. If you have a weak signal case, you may get lucky and test a spot with a high concentration of prions. But the opposite it true too; you can miss an infection by testing a sample with low concentrations. Western blot is much better for low signal situations.

4. The USDA in 2003 used the Western blot to confirm the BSE case in Washington state, and it sent samples to the U.K. for independent testing. In the case this November, which it announced was negative, it instead used the IHC test and did not send samples to the U.K. Is this good science?

It s not logical. If you have two consecutive questionable screenings, you do another test. I can only advise, it s management s duty at USDA to make the decisions. But when you have a discrepancy between the rapid test and the IHC, it is only logical to confirm it with another test.

5. We are hearing now about a new strain of BSE, atypical BSE or aBSE. Or BaSE. We have heard that IHC, the so-called gold standard, cannot detect the variant. Is this true?

Yes. There have been a few cases, one in Italy, one in Belgium, one here in France. It seems to only affect very old animals. The distribution in the brain is very different than we see with BSE, it looks very different. The IHC test will come back negative.

This his a very recent phenomenon. I have no opinion on its virulence. We do not know where it comes from. It could be a version of sporadic infection. Western blot caught them, but we would not even know it existed if we weren t running systematic testing in the EU.

BSE was around for a long time before we caught it and by then, it was everywhere. It had become highly infectious. It probably amplified due to low-temperature rendering. The disease was recycled through the food chain, and was given time to amplify. By the time it was identified, even good cooking couldn t eliminate it.

I can t stress enough that systematic testing is necessary. Withdrawing all positives from the food chain is the best way to break the cycle.

What can happen with testing of only cattle that are clearly at risk is that several can remain undetected. Canada has tested about 30,000 head of cattle and has three positives. That would indicate that there are probably undiscovered cases. And what happens then is that the disease is allowed to amplify. You have to maintain testing.

When people choose to protect their economic interests over public health, it can have a boomerang effect. It happened all through Europe. They always deny; it s not OUR problem, it is our neighbor s problem. And then a single case is discovered and the public reacts. The economic results are devastating. It would be better to just assume BSE is present and use systematic testing as protection. That way, the public is reassured that it is not entering the food supply.

By systematic testing, I mean doing as we do in the EU, which is to test every animal over 30 months of age when it is slaughtered. In Europe, three times as many cases of BSE have been caught by systematic testing as by clinical testing (of clearly sick animals). In 2004, eight clinical cases were discovered, 29 were discovered at rendering plants, and 17 at slaughter. We should be using these tests as a weapon to protect the public and to give them assurance that the food supply is being protected.

6. USDA s list of specified risk materials excludes some products, like blood and bone meal, that are banned in the EU and UK. Is our feed supply safe?

With SRMs, where do you stop? Tests have found prions in meat, nerves travel through meat, and so on. The main infectivity is in the brain and the spinal cord. A blood and bone meal ban in animal feed is not really necessary, because except in cases of highly infective animals, it is unlikely that they are dangerous in themselves. If you combine systematic testing and targeted SRM removal, the brain and the spinal column in cattle over 30 months, you can have a compromise that is both safer and less costly than expanded feed bans.

Certainly, you can stop the spread of BSE with a total ban on offal. But it has to be a total ban. It can t be given to sheep or swine or poultry. It would be very expensive and virtually impossible to accomplish. You can have farmers using the wrong feed or transportation errors.

Systematic testing makes far more sense. I think of it as a thermometer. It not only allows us to catch the disease, it also allows us to monitor its progress. We can watch the levels of infectivity and if they start going up instead of down, we can take measures.

To an extent, our environment is contaminated. About 10 percent of wild animals test positive for TSEs. If you recycle these agents, they can evolve and get more dangerous. This is probably what happened with BSE. It wasn t very dangerous until it evolved to the disease we know today.

People complain that testing is very expensive. It is much more expensive to kill and test whole herds.

7. In your opinion, is infected feed the sole method of transmission of BSE, apart from the very rare maternal transmission?

Feed is the main problem. However, we are seeing some other possibilities, including through fat and greases. Calves are fed milk extracts, with the cream removed. To make it nutritious, they are using fat and grease from cattle.

(FOLLOW QUESTION: Would that allow BSE to develop into an infective level in cattle younger than 30 months, assuming they might be getting infected at a younger age?)

8. You were involved in a study that tested two primates who were fed infected brain tissue. One eventually died of TSE; the other survived. The press reported that the main finding was that it would take something on the order of 1.5 kilograms of infected matter to create an infection, but that seems to be an oversimplification. Could you explain it further?

The findings suggest that as little as five grams is enough to infect. The 1.5 kilo figure is the amount of infected tissue that would have to be ingested from an animal that would be below the threshold of infection, and would test negative. In other words, even though a younger animal may be developing the disease, it would take a considerable amount of tissue to transmit the disease.

An animal could be just below the testing level, and not be particularly dangerous. But that is why you have to keep testing. Once it reaches the threshold, it can become highly infective.

9. BSE is a pretty horrifying disease, but overall, it has killed less than 200 humans, and only a handful in recent years. Listeria, by comparison, kills thousands every year. Overall, how do you rate the threat from BSE?

The overall risk is not particularly high. Over two million infected animals went into the food chain in Europe, 400,000 of them before the SRMs, the brains and spinal column, were removed from the carcass. Less than 200 died, and less than 4,000 are at risk of developing the disease. What we know now is that one particle is not going to kill you. There has to be condensation of the prions to be truly dangerous.

This is not a sterile world. But the danger is that now that the crisis appears to be over, attention will turn elsewhere and that will allow the disease to amplify again. Just as we stopped paying attention to AIDS when medication seemed to control it, then were surprised when a new and more infectious and aggressive strain appeared, we could be surprised by a more serious strain of BSE. That is why I support systematic testing for the long term. The object is to keep levels of BSE low, and to recognize the danger if it suddenly pops back up. ...END

TSS

######### https://listserv.kaliv.uni-karlsruhe.de/warc/bse-l.html ##########

-------- Original Message --------
Subject: hey there mike, some history on TERRY'S mad cow from TEXAS that was inconclusive ;-)
Date: Wed, 02 Feb 2005 16:24:22 -0600
From: "Terry S. Singeltary Sr."
To: hansmi@consumer.org CC: diane@prwatch.org, hallje@consumer.org

Mike,

for your files for a later date;-)

I WANT THAT TEXAS MAD COW!

follow the thread. moser of prionics is in it and Everet of TAHC.

SO close, BUT yet so damn far away...TSS

-------- Original Message --------
Subject: US CHOICE OF MAD COW TEST QUESTIONED
Date: Wed, 24 Mar 2004 16:12:06 -0600
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy
To: BSE-L@uni-karlsruhe.de

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

US CHOICE OF MAD COW TEST QUESTIONED

The US plans to measure the incidence of mad cow disease in its cattle with a test that its own officials have said gives too many false positives. Some experts fear the choice reflects an official desire to downplay the impact of the first positive BSE tests that emerge, when they turn out not to be confirmed.

Last week the US Department of Agriculture (USDA) approved two tests, including one made by the Californian firm BioRad, for screening up to 300,000 cattle for BSE, starting in July. No more tests will be licensed for months. Announcing the testing plan, chief veterinary officer Ron DeHaven cautioned that "there will be positive results", many of them false.

BioRad's antibody-based test for the prion protein that causes BSE has given numerous false positives in Belgium and Germany. And in Japan only 8 of 113 cattle that repeatedly tested positive with BioRad were confirmed by slower tests that do not give false positives.

The USDA even wrote last May that "it is well known" that tests like BioRad's give false positives. It states that other kinds of quick tests are more suitable for testing for very low levels of BSE, which are expected in the US.

The second quick test approved by the USDA, made by Maine-based IDEXX, could also in theory give false positives. It remains unclear how reliable it is, because there has been little practical experience with the test so far. It is not yet approved for use in Europe, where the vast majority of BSE tests are done.

Debora MacKenzie, Brussels correspondent, New Scientist. tel +32-2-245-0412 fax +32-2-245-0552 mobile +32-49-754-0444

http://www.newscientist.com/ =====================


Greetings,

odd that the USDA et al approves two US-OWNED tests that are _known_ to give false positives, when they know other rapid TSE test are much more reliable. IT's like they purposely do not want to find any TSE in the USA bovine, so they pick the worst test available. The USDA own experts think BioRad is not suitable for supposedly BSE/TSE free and low incidence areas, so why did they choose this test and or the IDEXX, which i dont think has even been submitted to the EU for evaluation and has no commercial experiance to my knowledge. You could almost get the feeling they are deliberately skipping over Prionics for the least supperior TSE rapid test. I believe the Canadians finally did choose prionics. maybe paul or marcus might comment? seems if North America is going to be a consolidated BEEF trading market amongst themselves and expect to export there tainted products everywhere, they could at least come up with the same TSE rapid Test. how can one use a less reliable test and the other use a more reliable test, and it all be the same? i know there is a word Dehaven used, but it slips my mind now, (consolidated markets) that's not it, but you get the just of my thoughts, i think;-)...TSS

########### http://mailhost.rz.uni-karlsruhe.de/warc/bse-l.html ############

-------- Original Message --------
Subject: Re: US CHOICE OF MAD COW TEST QUESTIONED
Date: Thu, 25 Mar 2004 00:53:39 +0100
From: Moser Markus
Reply-To: Bovine Spongiform Encephalopathy
To: BSE-L@uni-karlsruhe.de

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

Regarding your question about Canada's BSE-test choice for their official BSE surveillance, I can confirm that they chose the Prionics-Check Western rapid test. Regards Markus

-------- Original Message -------- Subject: Re: US CHOICE OF MAD COW TEST QUESTIONED
Date: Thu, 25 Mar 2004 01:11:04 +0100
From: Roland Heynkes
Reply-To: Bovine Spongiform Encephalopathy
To: BSE-L@uni-karlsruhe.de

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

Dear Terry,

odd that the USDA et al approves two US-OWNED tests that are _known_ to give false positives, when they know other rapid TSE test are much more reliable.

the BioRad-test seems to be the most sensitive rapid BSE test and it is clear that you "get" false positive results when you try to confirm its results with a less sensitive method like immune histochemistry. Poorly trained technicians of course may produce some false positives with the BioRad-test, but immune histochemistry produces many false negatives especially in the hands of not very experienced people. Generally the false negative and not the much fewer false positive results are the problem of all actually available BSE tests.

It is therefore not so easy to say, if the BioRad-test produced a false positive or if the confirming test produced a false negative result and which of them is more reliable. I for sure would not eat the meat of a cow which was seemingly false positive tested with the BioRad-test.

IT's like they purposely do not want to find any TSE in the USA bovine, so they pick the worst test available.

The BioRad-test is definitively not the worst test available (have a look on the EU results) and when a government does not want to get positive results, it uses immune histochemistry instead.

The USDA own experts think BioRad is not suitable for supposedly BSE/TSE free and low incidence areas, so why did they choose this test and or the IDEXX, which i dont think has even been submitted to the EU for evaluation and has no commercial experiance to my knowledge.

Are you sure that USDA has experts for BSE testing?

You could almost get the feeling they are deliberately skipping over Prionics for the least supperior TSE rapid test. I believe the Canadians finally did choose prionics. maybe paul or marcus might comment?

The Prionics western blot test is also a good rapid test which of course does not produce false positive results. In addition this test allows to see new variants of BSE, which would not be seen with the BioRad. But at least in Europe its positive results become confirmed by the OIE Western blot exactly as the BioRad results. Because of this control step the BioRad test cannot produce significantly more problems.

seems if North America is going to be a consolidated BEEF trading market amongst themselves and expect to export there tainted products everywhere, they could at least come up with the same TSE rapid Test. how can one use a less reliable test and the other use a more reliable test, and it all be the same? i know there is a word Dehaven used, but it slips my mind now, (consolidated markets) that's not it, but you get the just of my thoughts, i think;-)...TSS

Not the minor differences between the rapid tests are the problem, but the much to low testing numbers and the prefered IHC-testing in the USA. In Germany we test every month as many as the USA is going to test per year (mostly with BioRad) - and we have only 13 million cattle.

kind regards

Roland

########### http://mailhost.rz.uni-karlsruhe.de/warc/bse-l.html ############

-------- Original Message --------
Subject: Re: US CHOICE OF MAD COW TEST QUESTIONED
Date: Thu, 25 Mar 2004 02:51:09 +0100
From: Moser Markus
Reply-To: Bovine Spongiform Encephalopathy
To: BSE-L@uni-karlsruhe.de

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

Dear Roland Immunohistochemistry, correctly executed, is the gold standard, together with the OIE Western blotting method. It allows detection of infection even in cases where prion aggregates can only be detected in few individual cells. It is certainly not less sensitive than either Bio-Rad or Prionics. In fact, the abundant data on all three methods indicate equal diagnostic sensitivity (if sampling is done appropriate: note that immunohistochemistry has to be conducted on different tissue samples, since the tissue has to be formalin fixed). In case a BSE case obtained with a rapid test cannot be confirmed in a first approach with one of the gold standard methods, the second method will be used. I agree, that the sensitivity of immunohistochemistry can be negatively influenced e.g. by only looking at a limited number of slides or by not carefully examining the slides for prion aggregates. However, if a rapid test is not confirmed by immunohistochemistry due to a sloppy analysis, it will still show up in the OIE Western blot. Nevertheless, it is of course possible, that a true positive result cannot be confirmed e.g. if only the tissue sample used for the initial testing contained prion aggregates, which is theoretically possible, since the aggregates are not evenly distributed in the tissue. This is why it is not formally possible to disproof with 100% certainty an initial positive diagnosis (and you are right: it's certainly wise to rather not eat any suspicious animals). Nevertheless, false positives cannot in general be attributed to faulty confirmatory tests, but to the fact that the ELISA method simply produces a certain rate of false positives, which is why we offer rapid BSE tests on both platforms, the ELISA and the Western technology. And we make it clear to our customers, that when choosing the Prionics-Check LIA (the ELISA based test) coping with occasional false positive results will be inevitable. The LIA is therefore mostly used in European countries, with well established levels of BSE, while the Prionics-Check Western is also used in BSE-free countries (where a maximum positive predictive value is important to support the conclusion of low frequency or absence of BSE, which would otherwise be difficult for the reason you indicated and I mentioned above, i.e. due to the reason that it is hard to formally disprove an initial diagnosis with absolute certainty). Regards, Markus

-------- Original Message --------
Subject: Re: ''INCONCLUSIVE'' IS NEGATIVE or so they claim...OFFICIAL REPORT
Date: Tue, 1 Feb 2005 16:59:27 -0600
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy

To: BSE-L@LISTSERV.KALIV.UNI-KARLSRUHE.DE References: <41a3b789.6080907@wt.net> <41a4ed7c.4090501@wt.net>

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



Original Message --------

Subject: Re: BSE 'INCONCLUSIVE' COW from TEXAS ???
Date: Mon, 22 Nov 2004 21:07:51 -0600
From: "Terry S. Singeltary Sr."
To: Carla Everett References: <419e14e2.5040104@wt.net> <6.0.0.22.2.20041119113601.02682730@tahc.state.tx.us> <41a2724f.3000901@wt.net> <6.0.0.22.2.20041122174504.02796d38@tahc.state.tx.us> <41a27ebc.4050700@wt.net> <6.0.0.22.2.20041122183204.02801d88@tahc.state.tx.us>


ok, thank you Carla. i hate rumors and 'inconclusive' announcements. kind regards, terry Carla Everett wrote:

> our computer department was working on a place holder we could post

> USDA's announcement of any results. There are no results to be

> announced tonight

> by NVSL, so we are back in a waiting mode and will post the USDA

> announcement

> when we hear something.



> > > At 06:05 PM 11/22/2004, you wrote:

> >> why was the announcement on your TAHC site removed?

>> >> Bovine Spongiform Encephalopathy:

>> November 22: Press Release title here

>> >> star image More BSE information

>> >> >> >> terry


>> >> Carla Everett wrote: no confirmation on the U.S.' inconclusive test...

>>> no confirmation on location of animal.


I still want my Texas mad cows confirmed BY WB! TSS



-------- Original Message --------
Subject: Re: BSE 'INCONCLUSIVE' COW from TEXAS ???
Date: Mon, 22 Nov 2004 21:07:51 -0600
From: "Terry S. Singeltary Sr."
To: Carla Everett References: <419e14e2.5040104@wt.net> <6.0.0.22.2.20041119113601.02682730@tahc.state.tx.us> <41a2724f.3000901@wt.net> <6.0.0.22.2.20041122174504.02796d38@tahc.state.tx.us> <41a27ebc.4050700@wt.net> <6.0.0.22.2.20041122183204.02801d88@tahc.state.tx.us>

ok, thank you Carla. i hate rumors and 'inconclusive' announcements.

kind regards, terry

Carla Everett wrote:

our computer department was working on a place holder we could post USDA's announcement of any results. There are no results to be announced tonight by NVSL, so we are back in a waiting mode and will post the USDA announcement when we hear something.

At 06:05 PM 11/22/2004, you wrote:

why was the announcement on your TAHC site removed?

Bovine Spongiform Encephalopathy: November 22: Press Release title here star image More BSE information

terry

Carla Everett wrote:

no confirmation on the U.S.' inconclusive test... no confirmation on location of animal.

I still want my Texas mad cows confirmed BY WB!

TSS


http://www.usda.gov/wps/portal/usda/usdahome?contentidonly=true&contentid=2005/08/0336.xml



http://www.usda.gov/wps/portal/usda/usdahome?contentidonly=true&contentid=2005/08/0339.xml



http://www.usda.gov/documents/vs_bse_ihctestvar.pdf



http://www.usda.gov/wps/portal/usda/usdahome?contentidonly=true&contentid=2005/06/0217.xml





48 HOUR BSE TEST TURN AROUND TURNS INTO 7+ MONTHS $$$


http://www.usda.gov/wps/portal/usda/usdahome?contentidonly=true&contentid=2005/06/0218.xml



http://www.usda.gov/wps/portal/usda/usdahome?contentidonly=true&contentid=2005/06/0206.xml




ONE YEAR LATER, finally confirmed $$$


Release No. 0233.05 Contact: USDA Press Office (202) 720-4623

Printable version Email this page

TRANSCRIPT OF MEDIA CONFERENCE WITH REMARKS MADE BY AGRICULTURE SECRETARY MIKE JOHANNS, DR. JOHN CLIFFORD, CHIEF VETERINARY OFFICER, ANIMAL PLANT HEALTH INSPECTION SERVICE, AND DR. DANNY MATTHEWS, TSE PROGRAM MANAGER, VETERINARY LABORATORIES AGENCY, WEYBRIDGE, ENGLAND - WASHINGTON D.C. - JUNE 24, 2005


SNIP...



"So let me start first with the test results. As you are aware, last November we had an inconclusive report from a rapid screening test. USDA then conducted two IHC confirmatory tests, and both came out negative. A few weeks ago an additional confirmatory test was conducted, and that test is referred to as the Western blot test.

"On June 10 I learned that test was reactive and shared those results at that time.

"We now have the test results from the lab in Weybridge, England, as well as the results from additional testing in our own lab, and again I am here today to share those results with you.

"The results confirm the presence of BSE in this animal, an animal that was blocked from entering the food supply thanks to the firewalls that are in place. It is critically important to note that this animal was identified as a high risk animal. A sample was taken, and the carcass was incinerated.

http://www.usda.gov/wps/portal/usda/usdahome?contentidonly=true&contentid=2005/06/0233.xml




http://madcowtesting.blogspot.com/2008/01/bse-oie-usda.html




Tuesday, July 14, 2009

U.S. Emergency Bovine Spongiform Encephalopathy Response Plan Summary and BSE Red Book Date: February 14, 2000 at 8:56 am PST

WHERE did we go wrong $$$


http://madcowtesting.blogspot.com/2009/07/us-emergency-bovine-spongiform.html





TSS

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