Wednesday, May 5, 2010

Scientific Opinion on Analytical sensitivity of approved TSE rapid tests – new data for assessment of two rapid tests

Scientific Opinion on Analytical sensitivity of approved TSE rapid tests – new data for assessment of two rapid tests Question number: EFSA-Q-2010-00114

Adopted: 22 April 2010

Summary (0.1 Mb)

Opinion (0.1 Mb)

Annex (2.5 Mb)


Following a request from the European Commission, the Panel on Biological Hazards (BIOHAZ) was asked to deliver a scientific opinion on analytical sensitivity of approved TSE rapid tests – new data for assessment of two rapid tests.

On 18 December 2009 EFSA published a Scientific Opinion on analytical sensitivity of approved TSE rapid tests. With regard to approved rapid tests for the detection of BSE in cattle, the Opinion concluded that, during a comparative analytical sensitivity study performed by the Community Reference Laboratory (CRL) for TSEs, the two rapid tests, Prionics®-Check LIA and Prionics®-Check PrioSTRIP, gave unexplained and unresolved specificity problems which hampered the interpretation of their analytical sensitivity. On this basis, the BIOHAZ Panel recommended that the analytical sensitivity of those two tests with cattle BSE samples should be re-assessed by appropriate experiments, under the supervision of the CRL. Following this recommendation, a new study (“re-assessment study”) was submitted for evaluation by the European Commission to EFSA. This Opinion provides a scientific assessment of the re-assessment study and provides conclusions on the analytical sensitivity of the two above rapid tests with regard to cattle BSE.

The BIOHAZ Panel concludes that the experimental design used in the new study is scientifically sound and can be considered equivalent to that applied during the first CRL study. The study was not hampered by specificity problems and allowed the re-assessment of the analytical sensitivity of Prionics®-Check LIA and Prionics®-Check PrioSTRIP with cattle BSE samples. The two tests performed within a maximal 2 log10 inferiority range as compared to the most sensitive test system identified in the first CRL study, as set out in the current EFSA protocols for the evaluation of TSE rapid post mortem tests.

The BIOHAZ Panel further concludes that the precise causes of the initial reactives in negative control samples observed in the first CRL study with the two rapid tests remain unidentified, since the re-assessment study was not designed for investigating them.

Published: 29 April 2010

Wednesday, December 23, 2009

Scientific Opinion on Analytical sensitivity of approved TSE rapid tests Scientific Opinion on Analytical sensitivity of approved TSE rapid tests Question number: EFSA-Q-2009-00687 Adopted: 10 December 2009 Summary (32 KB)

Opinion (417 KB)

Annex – Report of the CRL study (762 KB)

Thursday, October 18, 2007


Subject: Re: USDA VS CREEKSTONE BSE/BASE/TSE TESTING Civil Action No. 06-0544

From: "Terry S. Singeltary Sr."

Reply-To: Bovine Spongiform Encephalopathy

Date: Wed, 5 Sep 2007 09:00:11 -0500

Content-Type: text/plain

Parts/Attachments: text/plain (554 lines)


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

Subject: RE: Questions on your testing plans.
Date: Mon, 9 Apr 2007 13:01:30 -0500
From: Joe B. Meng To: CC: References:


As of our most recent conversations, it is still our intent to test every animal.

The testing would be uniform for all programs.

Our certification for all Creekstone brands (Premium, Natural and International) currently requires an "A" maturity animal. These are considered to be 30 months and younger as determined by detention. It has been our experience that this system errs on the side of caution as we have had numerous age-verified animals well under 30 months to be excluded based on detention. All countries to which we export, except Japan, require under 30 months and have approved the detention process.

We are asking that USDA and FSIS supervise all testing at our expense and any inconclusive would be sent to Ames, IA for confirmatory testing. Once they have a questionable sample, the same procedures will be followed that are currently approved. In the past, that has included announcing the inconclusive as well as the final result. As you know, the two native born cases were determined to be atypical, but I don't believe that was announced at the same time as the positive results were announced, so I'm not certain on USDA policy for announcing the strain.

We have had conversations with both BioRad and IDEXX, both of which are approved by USDA. Most of the equipment in the lab is from BioRad, but some of that would need to be replaced with updated equipment. I have met with representatives of both companies and they tell me we could have the new equipment in place and personnel training updated inside of two weeks. Both companies would keep people on site for the early stages of testing. The lab has already been approved so we could be ready fairly quickly unless USDA finds a way to complicate the process. Additionally, both BioRad and IDEXX have looked at the facility and tell us it is superior to the currently approved facilities.

Joe Bill


Friday, August 29, 2008



14th International Congress on Infectious Diseases H-type and L-type Atypical BSE January 2010 (special pre-congress edition)

18.173 page 189

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

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

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

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

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

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


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.


12 years independent research of available data


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.


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.

see page 114 ;

Sunday, April 4, 2010


position: Post Doctoral Fellow Atypical BSE in Cattle

Closing date: December 24, 2009

Anticipated start date: January/February 2010

Employer: Canadian and OIE Reference Laboratories for BSE CFIA Lethbridge Laboratory, Lethbridge/Alberta


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.


Wednesday, March 31, 2010

Atypical BSE in Cattle

Monday, October 19, 2009

Atypical BSE, BSE, and other human and animal TSE in North America Update October 19, 2009


I ask Professor Kong ;

Thursday, December 04, 2008 3:37 PM Subject: RE: re--Chronic Wating Disease (CWD) and Bovine Spongiform Encephalopathies (BSE): Public Health Risk Assessment

''IS the h-BSE more virulent than typical BSE as well, or the same as cBSE, or less virulent than cBSE? just curious.....''

Professor Kong reply ;


''As to the H-BSE, we do not have sufficient data to say one way or another, but we have found that H-BSE can infect humans. I hope we could publish these data once the study is complete.

Thanks for your interest.''

Best regards,

Qingzhong Kong, PhD Associate Professor Department of Pathology Case Western Reserve University Cleveland, OH 44106 USA


I look forward to further transmission studies, and a true ENHANCED BSE/atypical BSE surveillance program put forth testing all cattle for human and animal consumption for 5 years. a surveillance program that uses the most sensitive TSE testing, and has the personnel that knows how to use them, and can be trusted. I look forward to a stringent mad cow feed ban being put forth, and then strictly enforced. we need a forced, not voluntary feed ban, an enhanced feed ban at that, especially excluding blood. we need some sort of animal traceability. no more excuses about privacy. if somebody is putting out a product that is killing folks and or has the potential to kill you, then everybody needs to know who they are, and where that product came from. same with hospitals, i think medical incidents in all states should be recorded, and made public, when it comes to something like a potential accidental transmission exposure event. so if someone is out there looking at a place to go have surgery done, if you have several hospitals having these type 'accidental exposure events', than you can go some place else. it only makes sense. somewhere along the road, the consumer lost control, and just had to take whatever they were given, and then charged these astronomical prices. some where along the line the consumer just lost interest, especially on a long incubating disease such as mad cow disease i.e. Transmissible Spongiform Encephalopathy. like i said before, there is much more to the mad cow story than bovines and eating a hamburger, we must start focusing on all TSE in all species. ...TSS

Archive Number 20100405.1091 Published Date 05-APR-2010

Subject PRO/AH/EDR> Prion disease update 1010 (04)


[Terry S. Singeltary Sr. has added the following comment:

"According to the World Health Organisation, the future public health threat of vCJD in the UK and Europe and potentially the rest of the world is of concern and currently unquantifiable. However, the possibility of a significant and geographically diverse vCJD epidemic occurring over the next few decades cannot be dismissed


The key word here is diverse. What does diverse mean? If USA scrapie transmitted to USA bovine does not produce pathology as the UK c-BSE, then why would CJD from there look like UK vCJD?",F2400_P1001_PUB_MAIL_ID:1000,82101

Monday, March 29, 2010


> Up until about 6 years ago, the pt worked at Tyson foods where she worked

> on the assembly line, slaughtering cattle and preparing them for

> packaging. She was exposed to brain and spinal cord matter when she would

> euthanize the cattle.


2008 - 2010

The statistical incidence of CJD cases in the United States has been revised to reflect that there is one case per 9000 in adults age 55 and older. Eighty-five percent of the cases are sporadic, meaning there is no known cause at present.


5 Includes 41 cases in which the diagnosis is pending, and 17 inconclusive cases; 6 Includes 46 cases with type determination pending in which the diagnosis of vCJD has been excluded.

Saturday, January 2, 2010

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

my comments to PLosone here ;

please see full text ;

Friday, February 05, 2010

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

Wednesday, April 28, 2010





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