Ridley Agrees to Settlement in Canadian BSE Lawsuit

[flounder]

Flounder,

Given that this is the first I've heard of the 2004 Texas downer, I have no real idea what type BSE it may be, if at all, but my wild guess would be H-type which is known to exist in Texas. If they still have the tissue frozen somewhere, all it takes is the will to find out for sure. Monoclonal antibodies are funny that way.

Where do you get the idea that H-type is more virulent for humans? It is less virulent in cattle, so that seems counter-intuitive.

your not reading what i have already posted. there is nothing left to test.
that was the objective of rendering whole cow with no test at all.


as far as the atypicals being more virulent ;


P02.35 Molecular Features of the Protease-resistant Prion Protein (PrPres)
in H- type BSE

Biacabe, A-G1; Jacobs, JG2; Gavier-Widén, D3; Vulin, J1; Langeveld, JPM2;
Baron, TGM1 1AFSSA, France; 2CIDC-Lelystad, Netherlands; 3SVA, Sweden

Western blot analyses of PrPres accumulating in the brain of BSE- infected
cattle have demonstrated 3 different molecular phenotypes regarding to the
apparent molecular masses and glycoform ratios of PrPres bands. We initially
described isolates (H-type BSE) essentially characterized by higher PrPres
molecular mass and decreased levels of the diglycosylated PrPres band, in
contrast to the classical type of BSE. This type is also distinct from
another BSE phenotype named L-type BSE, or also BASE (for Bovine Amyloid
Spongiform Encephalopathy), mainly characterized by a low representation of
the diglycosylated PrPres band as well as a lower PrPres molecular mass.
Retrospective molecular studies in France of all available BSE cases older
than 8 years old and of part of the other cases identified since the
beginning of the exhaustive surveillance of the disease in 20001 allowed to
identify 7 H- type BSE cases, among 594 BSE cases that could be classified
as classical, L- or H-type BSE. By Western blot analysis of H-type PrPres,
we described a remarkable specific feature with antibodies raised against
the C-terminal region of PrP that demonstrated the existence of a more
C-terminal cleaved form of PrPres (named PrPres#2 ), in addition to the
usual PrPres form (PrPres #1). In the unglycosylated form, PrPres #2
migrates at about 14 kDa, compared to 20 kDa for PrPres #1. The proportion
of the PrPres#2 in cattle seems to by higher compared to the PrPres#1.
Furthermore another PK–resistant fragment at about 7 kDa was detected by
some more N-terminal antibodies and presumed to be the result of cleavages
of both N- and C- terminal parts of PrP. These singular features were
maintained after transmission of the disease to C57Bl/6 mice. The
identification of these two additional PrPres fragments (PrPres #2 and 7kDa
band)
*** reminds features reported respectively in sporadic Creutzfeldt-Jakob
disease and in Gerstmann-Sträussler-Scheinker (GSS) syndrome in humans.


FC5.5.1 BASE Transmitted to Primates and MV2 sCJD Subtype Share PrP27-30 and
PrPSc C-terminal Truncated Fragments


Zanusso, G1; Commoy, E2; Fasoli, E3; Fiorini, M3; Lescoutra, N4; Ruchoux,
MM4; Casalone, C5; Caramelli, M5; Ferrari, S3; Lasmezas, C6; Deslys, J-P4;
Monaco, S3 1University of Verona, of Neurological and Visual Sciences,
Italy; 2CEA, IMETI/SEPIA, France; 3University of Verona, Neurological and
Visual Sciences, Italy; 4IMETI/SEPIA, France; 5IZSPLVA, Italy; 6The Scripps
Research Insitute, USA

The etiology of sporadic Creutzfeldt-Jakob disease (sCJD), the most frequent
human prion disease, remains still unknown. The marked disease phenotype
heterogeneity observed in sCJD is thought to be influenced by the type of
proteinase K- resistant prion protein, or PrPSc (type 1 or type 2 according
to the electrophoretic mobility of the unglycosylated backbone), and by the
host polymorphic Methionine/Valine (M/V) codon 129 of the PRNP. By using a
two-dimensional gel electrophoresis (2D-PAGE) and imunoblotting we
previously showed that in sCJD, in addition to the PrPSc type, distinct
PrPSc C-terminal truncated fragments (CTFs) correlated with different sCJD
subtypes. Based on the combination of CTFs and PrPSc type, we distinguished
three PrPSc patterns: (i) the first was observed in sCJD with PrPSc type 1
of all genotypes,;

(ii) the second was found in M/M-2 (cortical form); (iii) the third in
amyloidogenic M/V- 2 and V/V-2 subtypes (Zanusso et al., JBC 2004) .
Recently, we showed that sCJD subtype M/V-2 shared molecular and
pathological features with an atypical form of BSE, named BASE, thus
suggesting a potential link between the two conditions. This connection was
further confirmed after 2D-PAGE analysis, which showed an identical PrPSc
signature, including the biochemical pattern of CTFs. To pursue this issue,
we obtained brain homogenates from Cynomolgus macaques intracerebrally
inoculated with brain homogenates from BASE. Samples were separated by using
a twodimensional electrophoresis (2D-PAGE) followed by immunoblotting. We
here show that the PrPSc pattern obtained in infected primates is identical
to BASE and sCJD MV-2 subtype.
*** These data strongly support the link, or at least a common ancestry,
between a sCJD subtype and BASE.

This work was supported by Neuroprion (FOOD-CT-2004-506579)

************************************************** *****

USA MAD COW CASES IN ALABAMA AND TEXAS

***PLEASE NOTE***

USA BASE CASE, (ATYPICAL BSE), AND OR TSE (whatever they are calling it
today), please note that both the ALABAMA COW, AND THE TEXAS COW,both were
''H-TYPE'', personal communication Detwiler et al Wednesday, August 22, 2007
11:52 PM. ...TSS

http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0708&L=sanet-mg&T=0&P=19779


************************************************** *****

FC5.5.2 Transmission of Italian BSE and BASE Isolates in Cattle Results into
a Typical BSE Phenotype and a Muscle Wasting Disease

Zanusso, G1; Lombardi, G2; Casalone, C3; D'Angelo, A4; Gelmetti, D2;
Torcoli, G2; Barbieri, I2; Corona, C3; Fasoli, E1; Farinazzo, A1; Fiorini,
M1; Gelati, M1; Iulini, B3; Tagliavini, F5; Ferrari, S1; Monaco, S1;
Caramelli, M3; Capucci, L2 1University of Verona, Neurological and Visual
Sciences, Italy; 2IZSLER, Italy; 3IZSPLVA, Italy; 4University of Turin,
Animal Pathology, Italy; 5Isituto Carlo Besta, Italy

The clinical phenotype of bovine spongiform encephalopathy has been
extensively reported in early accounts of the disorder. Following the
introduction of statutory active surveillance, almost all BSE cases have
been diagnosed on a pathological/molecular basis, in a pre-symptomatic
clinical stage. In recent years, the active surveillance system has
uncovered atypical BSE cases, which are characterized by distinct conformers
of the PrPSc, named high-type (BSE-H) and low-type (BSE-L), whose
clinicopathological phenotypes remain unknown. We recently reported two
Italian atypical cases with a PrPSc type similar to BSE-L, pathologically
characterized by PrP amyloid plaques. Experimental transmission to TgBov
mice has recently disclosed that BASE is caused by a distinct prion strain
which is extremely virulent. A major limitation of transmission studies to
mice is the lack of reliable information on clinical phenotype of BASE in
its natural host. In the present study, we experimentally infected
Fresian/Holstein and Alpine/Brown cattle with Italian BSE and BASE isolates
by i.c. route. BASE infected cattle showed survival times significantly
shorter than BSE, a finding more readily evident in Fresian/Holstein, and in
keeping with previous observations in TgBov mice. Clinically, BSE-infected
cattle developed a disease phenotype highly comparable with that described
in field BSE cases and in experimentally challenged cattle. On the contrary,
BASE-inoculated cattle developed an amyotrophic disorder accompanied by
mental dullness. The molecular and neuropathological profiles, including PrP
deposition pattern, closely matched those observed in the original cases.
This study further confirms that BASE is caused by a distinct prion isolate
and discloses a novel disease phenotype in cattle, closely resembling the
phenotype previous reported in scrapie-inoculated cattle
*** and in some subtypes of inherited and sporadic Creutzfeldt-Jakob
disease.

Oral Abstracts 14



snip...



P04.27

Experimental BSE Infection of Non-human Primates: Efficacy of the Oral Route

Holznagel, E1; Yutzy, B1; Deslys, J-P2; Lasmézas, C2; Pocchiari, M3;
Ingrosso, L3; Bierke, P4; Schulz-Schaeffer, W5; Motzkus, D6; Hunsmann, G6;
Löwer, J1 1Paul-Ehrlich-Institut, Germany; 2Commissariat à l´Energie
Atomique, France; 3Instituto Superiore di Sanità, Italy; 4Swedish Institute
for Infectious Disease control, Sweden; 5Georg August University, Germany;
6German Primate Center, Germany

Background:

In 2001, a study was initiated in primates to assess the risk for humans to
contract BSE through contaminated food. For this purpose, BSE brain was
titrated in cynomolgus monkeys.

Aims:

The primary objective is the determination of the minimal infectious dose
(MID50) for oral exposure to BSE in a simian model, and, by in doing this,
to assess the risk for humans. Secondly, we aimed at examining the course of
the disease to identify possible biomarkers.

Methods:

Groups with six monkeys each were orally dosed with lowering amounts of BSE
brain: 16g, 5g, 0.5g, 0.05g, and 0.005g. In a second titration study,
animals were intracerebrally (i.c.) dosed (50, 5, 0.5, 0.05, and 0.005 mg).

Results:

In an ongoing study, a considerable number of high-dosed macaques already
developed simian vCJD upon oral or intracerebral exposure or are at the
onset of the clinical phase. However, there are differences in the clinical
course between orally and intracerebrally infected animals that may
influence the detection of biomarkers.

Conclusions:

Simian vCJD can be easily triggered in cynomolgus monkeys on the oral route
using less than 5 g BSE brain homogenate. The difference in the incubation
period between 5 g oral and 5 mg i.c. is only 1 year (5 years versus 4
years). However, there are rapid progressors among orally dosed monkeys that
develop simian v CJD as fast as intracerebrally inoculated animals.

The work referenced was performed in partial fulfilment of the study "BSE in
primates" supported by the EU (QLK1-2002-01096).

http://www.prion2007.com/pdf/Prion%20Book%20of%20Abstracts.pdf


Subject: Aspects of the Cerebellar Neuropathology in Nor98

Date: September 26, 2007 at 4:06 pm PST

P03.141

Aspects of the Cerebellar Neuropathology in Nor98

Gavier-Widén, D1; Benestad, SL2; Ottander, L1; Westergren, E1 1National
Veterinary Insitute, Sweden; 2National Veterinary Institute, Norway

Nor98 is a prion disease of old sheep and goats. This atypical form of
scrapie was first described in Norway in 1998. Several features of Nor98
were shown to be different from classical scrapie including the distribution
of disease associated prion protein (PrPd) accumulation in the brain. The
cerebellum is generally the most affected brain area in Nor98. The study
here presented aimed at adding information on the neuropathology in the
cerebellum of Nor98 naturally affected sheep of various genotypes in Sweden
and Norway. A panel of histochemical and immunohistochemical (IHC) stainings
such as IHC for PrPd, synaptophysin, glial fibrillary acidic protein,
amyloid, and cell markers for phagocytic cells were conducted. The type of
histological lesions and tissue reactions were evaluated. The types of PrPd
deposition were characterized. The cerebellar cortex was regularly affected,
even though there was a variation in the severity of the lesions from case
to case. Neuropil vacuolation was more marked in the molecular layer, but
affected also the granular cell layer. There was a loss of granule cells.
Punctate deposition of PrPd was characteristic. It was morphologically and
in distribution identical with that of synaptophysin, suggesting that PrPd
accumulates in the synaptic structures. PrPd was also observed in the
granule cell layer and in the white matter.
*** The pathology features of Nor98 in the cerebellum of the affected sheep
showed similarities with those of sporadic Creutzfeldt-Jakob disease in
humans.

http://www.prion2007.com/pdf/Prion%20Book%20of%20Abstracts.pdf


SEE FULL TEXT ;

Creutzfeldt Jakob Disease Delaware UPDATE

http://cjdmadcowbaseoct2007.blogspot.com/2008/02/creutzfeldt-jakob-disease-delaware.html


Creutzfeldt Jakob Disease Texas

http://cjdtexas.blogspot.com/


USDA CERTIFIED H-BASE MAD COW SCHOOL LUNCH PROGRAM


http://cjdmadcowbaseoct2007.blogspot.com/2008/02/usda-certified-h-base-mad-cow-school.html



18 January 2007 - Draft minutes of the SEAC 95 meeting (426 KB) held on 7
December 2006 are now available.


snip...



64. A member noted that at the recent Neuroprion meeting, a study was
presented showing that in transgenic mice BSE passaged in sheep may be more
virulent and infectious to a wider range of species than bovine derived BSE.

Other work presented suggested that BSE and bovine amyloidotic spongiform
encephalopathy (BASE) MAY BE RELATED. A mutation had been identified in the
prion protein gene in an AMERICAN BASE CASE THAT WAS SIMILAR IN NATURE TO A
MUTATION FOUND IN CASES OF SPORADIC CJD.


snip...



http://www.seac.gov.uk/minutes/95.pdf




3:30 Transmission of the Italian Atypical BSE (BASE) in Humanized Mouse

Models Qingzhong Kong, Ph.D., Assistant Professor, Pathology, Case Western Reserve
University

Bovine Amyloid Spongiform Encephalopathy (BASE) is an atypical BSE strain
discovered recently in Italy, and similar or different atypical BSE cases
were also reported in other countries. The infectivity and phenotypes of
these atypical BSE strains in humans are unknown. In collaboration with
Pierluigi Gambetti, as well as Maria Caramelli and her co-workers, we have
inoculated transgenic mice expressing human prion protein with brain
homogenates from BASE or BSE infected cattle. Our data shows that about half
of the BASE-inoculated mice became infected with an average incubation time
of about 19 months; in contrast, none of the BSE-inoculated mice appear to
be infected after more than 2 years.

***These results indicate that BASE is transmissible to humans and suggest that BASE is more virulent than
classical BSE in humans.***


6:30 Close of Day One


http://www.healthtech.com/2007/tse/day1.asp




SEE STEADY INCREASE IN SPORADIC CJD IN THE USA FROM
1997 TO 2006. SPORADIC CJD CASES TRIPLED, with phenotype
of 'UNKNOWN' strain growing. ...


http://www.cjdsurveillance.com/resources-casereport.html



There is a growing number of human CJD cases, and they were presented last
week in San Francisco by Luigi Gambatti(?) from his CJD surveillance
collection.

He estimates that it may be up to 14 or 15 persons which display selectively
SPRPSC and practically no detected RPRPSC proteins.


http://www.fda.gov/ohrms/dockets/ac/06/transcripts/1006-4240t1.htm


http://www.fda.gov/ohrms/dockets/ac/06/transcripts/2006-4240t1.pdf



Thursday, January 31, 2008

Evaluation of the Human Transmission Risk of an Atypical Bovine Spongiform
Encephalopathy Prion Strain

J. Virol. doi:10.1128/JVI.02561-07
Copyright (c) 2008, American Society for Microbiology and/or the Listed
Authors/Institutions.
All Rights Reserved.



snip...


These results suggest that, in
humans, BASE is a more virulent BSE strain and likely lymphotropic.


http://jvi.asm.org/cgi/content/abstract/JVI.02561-07v1?papetoc



for those interested, further into this study ;

http://cjdmadcowbaseoct2007.blogspot.com/2008/02/evaluation-of-human-transmission-risk.html



Tissue distribution. For atypical scrapie, what is PrPres and
infectivity distribution within sheep of different genotypes,
particularly with respect to SRM removal? For classical
scrapie and experimental BSE in sheep, tissue distribution of
infectivity is widespread. Thus, even with SRM controls in
place, an infected sheep poses around 1000 times the risk to
human health than does an infected cow22. Does the
distribution depend on whether infection is by the oral or
21 Gubbins S. Prevalence of BSE in sheep: interpreting the results of
retrospective and
prospective testing of sheep TSE cases. SEAC 84 open meeting
22 paper presented to Food Standards Agency board on 9 December 2004.
http://www.foodstandards.gov.uk/multimedia/pdfs/fsa041204.pdf
Also see paper SEAC/84/2 Annex 2: McLean, A.
Page 13
© SEAC 27 February 2006
intracerebral route? Are some VRQ sheep carriers with no
neurological symptoms?



SEAC SHEEP SUBGROUP
POSITION STATEMENT


http://www.seac.gov.uk/pdf/positionstatement-sheep-subgroup.pdf


NOR-98 ATYPICAL SCRAPIE USA UPDATE AS AT OCT 2007

http://nor-98.blogspot.com/


SCRAPIE USA

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



there are over 20+ strains of typical scrapie, there are atypical scrapie i.e. nor-98 (five documented cases in the USA), of which pathology is very similar to sporadic CJD in humans, CWD (science shows different strains likely), of deer and elk, proven BSE, h-BASE in n. America, TME as well, all of which have been rendered and fed to livestock for human and animal consumption. different routes, i.e. direct tainted feed, cross contamination, different titres of infectivity, DOSE, etc, the likelyhood of one single strain in the US in is not logical. only in USDA's dreams $$$


TSS

 

[Shaft]

That material is being held by the firm, which is cooperating fully with FDA.

I presume now that the material is no longer being held, but my presumptions have been wrong before. That is the nature of presumptions, after all. What was the age of the downer? That could be indicative of the strain of prion involved, if any.

With respect, the very interesting paper presented last year in Cambridge and recently printed in the Journal of Virology "suggests that BASE is a more virulent strain and likely lymphotrophic."

BASE is also known as L-type BSE:

"Two atypical BSE strains, BASE (or BSE-L) and BSE-H, have been discovered in several countries since 2004." (from the same abstract)

To my knowledge BASE has not been confirmed to date in North America.

However, I agree that the fact that H-type does not appear transmissible to mink certainly raises the question as to the origin of reported TME in the fifties through the eighties in NA.

Could it be that we exported BSE to the UK and they sent it back after passage through sheep?

No having fun.

 

[flounder]

With respect, the very interesting paper presented last year in Cambridge and recently printed in the Journal of Virology "suggests that BASE is a more virulent strain and likely lymphotrophic."

BASE is also known as L-type BSE:

"Two atypical BSE strains, BASE (or BSE-L) and BSE-H, have been discovered in several countries since 2004." (from the same abstract)

To my knowledge BASE has not been confirmed to date in North America.


snip...

shaft my man, where have you been :???:


the last two mad cows in the USA i.e. Alabama and Texas
(the confirmed mad cow in Texas, NOT the mad cow that got away$),
but both those mad cows were of the h-BASE atypical BSE strain, call it what you wish, i don't think the science community as a whole have come to a single terminology just yet, but these are he facts, both were h-BASE ;


***PLEASE NOTE***

USA BASE CASE, (ATYPICAL BSE), AND OR TSE (whatever they are calling it today), please note that both the ALABAMA COW, AND THE TEXAS COW,both were ''H-TYPE'', personal communication Detwiler et al Wednesday, August 22, 2007 11:52 PM. ...TSS

http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0708&L=sanet-mg&T=0&P=19779



Since these 2 publications additional cases of atypical BSE have been found in other countries. H cases have been detected in Canada, France, Germany, Japan, the Netherlands, Poland, Sweden, Switzerland and the United States. L cases have been diagnosed in Belgium, Denmark,
France, Germany, Italy, Japan and Poland (Brown et al., 2006). The L cases in Belgium and Japan had additional differences (Yamakawa et al., 2003; De Bosschere et al., 2004). Two important points must be emphasized regarding the atypical BSE cases. Information regarding
lesion pattern and PrP distribution is very limited as most cases were detected by the large scale surveillance programs which only required collection of the brain stem. In addition, if countries were using certain tests, some cases of atypical BSE may have been misdiagnosed or reported as negative. For example, if a country relied solely on immunohistochemistry to confirm positive ELISA screening test cases and did not use western blotting at all, the banding pattern differences would go unnoticed.


http://www.usaha.org/committees/reports/2006/report-fe-2006.pdf


with that said, there have also been 5 documented cases of the atypical scrapie NOR-98 documented in the USA in 2007, in 5 different states ;


In FY 2007, 331 scrapie cases have been confirmed and reported by the National Veterinary Services Laboratories (NVSL), including 59* Regulatory Scrapie Slaughter Surveillance (RSSS) cases (Figure 5 and Slide 16). In FY 2007, two field cases, one validation case, and two RSSS cases were consistent with Nor-98 scrapie. The Nor98-like cases originated from flocks in California, Minnesota, Colorado, Wyoming and Indiana respectively. Nineteen cases of scrapie in goats have been reported since 1990 (Figure 6). The last goat case was reported in September 2007.


snip...


see full report here ;


http://www.aphis.usda.gov/animal_health/animal_diseases/scrapie/downloads/yearly_report.pps



P03.141

Aspects of the Cerebellar Neuropathology in Nor98

Gavier-Widén, D1; Benestad, SL2; Ottander, L1; Westergren, E11National Veterinary Insitute, Sweden; 2National Veterinary Institute, Norway

Nor98 is a prion disease of old sheep and goats. This atypical form of scrapie was first described in Norway in 1998. Several features of Nor98 were shown to be different from classical scrapie including the distribution of disease associated prion protein (PrPd) accumulation in the brain. The cerebellum is generally the most affected brain area in Nor98. The study here presented aimed at adding information on the neuropathology in the cerebellum of Nor98 naturally affected sheep of various genotypes in Sweden and Norway. A panel of histochemical and immunohistochemical (IHC) stainings such as IHC for PrPd, synaptophysin, glial fibrillary acidic protein,amyloid, and cell markers for phagocytic cells were conducted. The type of histologicallesions and tissue reactions were evaluated. The types of PrPd deposition were characterized. The cerebellar cortex was regularly affected, even though there was avariation in the severity of the lesions from case to case. Neuropil vacuolation was more marked in the molecular layer, but affected also the granular cell layer. There wasa loss of granule cells. Punctate deposition of PrPd was characteristic. It was morphologically and in distribution identical with that of synaptophysin, suggesting that PrPd accumulates in the synaptic structures. PrPd was also observed in the granule cell layer and in the white matter. The pathology features of Nor98 in the cerebellum of the affected sheep showed similarities with those of sporadic Creutzfeldt-Jakob disease in humans.


http://www.prion2007.com/pdf/Prion%20Book%20of%20Abstracts.pdf

Could it be that we exported BSE to the UK and they sent it back after passage through sheep?

yes i believe this possible, you cannot rule this out completely.


also, the USA developed the continuous rendering technology with low temps, THEN shipped that technology to the UK where they used it first for about 5 years, before we started using it ;


The exact same recipe for B.S.E. existed in the U.S. for years and years. In reading over the Qualitative Analysis of BSE Risk Factors-1, this is a 25 page report by the USDA:APHIS:VS. It could have been done in one page. The first page, fourth paragraph says it all;

"Similarities exist in the two countries usage of continuous rendering technology and the lack of usage of solvents, however, large differences still remain with other risk factors which greatly reduce the potential risk at the national level."

Then, the next 24 pages tries to down-play the high risks of B.S.E. in the U.S., with nothing more than the cattle to sheep ratio count, and the geographical locations of herds and flocks. That's all the evidence they can come up with, in the next 24 pages.

Something else I find odd, page 16;

"In the United Kingdom there is much concern for a specific continuous rendering technology which uses lower temperatures and accounts for 25 percent of total output. This technology was _originally_ designed and imported from the United States. However, the specific application in the production process is _believed_ to be different in the two countries."

A few more factors to consider, page 15;


snip...end


2 January 2000

British Medical Journal

U.S. Scientist should be concerned with a CJD epidemic in the U.S., as well

http://www.bmj.com/cgi/eletters/320/7226/8/b#6117


15 November 1999

British Medical Journal

vCJD in the USA * BSE in U.S.


http://www.bmj.com/cgi/eletters/319/7220/1312/b#5406


my God, have i been sitting here this long :shock: :arrow: :cry2: :help:


TSS

 

[Shaft]

TSS,

What we have here is a difference in our understanding of terminological exactitude (unlike Coolhand Luke whose problem was failure to communicate). The term BASE, as I understand it, refers strictly to L-type BSE and does not encompass H-type BSE. This is the understanding of the terminology as presented in the transmission study in the January edition of the Journal of Virology. This is also the understanding of the terminology of all of the scientific papers you have cited so far.

Forgive me for being anal about precision in scientific terminology, but we are all the products of our training. Besides, I refer personally to H-type as 'background" BSE (BBSE) to avoid the confusion and to reflect my belief that H-type BSE has been around in NA for a long, long time.

Using this terminology BASE has so far not been confirmed in NA to my knowledge.

"Japan, the USA, Canada and several European countries (including France, the Netherlands, Sweden, Switzerland, and Germany) have reported H-type BSE. Japan and several European countries (including Italy, Denmark, Poland, Belgium and Germany) have reported L-type BSE. Both types have been reported predominantly in cattle over 10 years old. In both types, the abnormal prion protein (PrP Sc ) in these animals has different biochemical characteristics to that seen in BSE. Mice experimentally infected with the brains of these animals develop a disease which differs from that seen in BSE infected mice. In two L-type cases where the intact whole brain was studied, the pattern of deposition of PrP Sc in the brain differed from that in BSE."

http://www.defra.gov.uk/news/2007/070309b.htm

On a not wholly unrelated note, it was only a matter of time until someone came up with a potential treatment regimen, or at least a means of slowing down CNS destruction by the (various?) BSE prions.

http://vir.sgmjournals.org/cgi/content/abstract/89/2/594

Memantine is an Alzheimer's treatment drug manufactured by Merz (not a typo). Stock up today.

 

[flounder]

TSS,

What we have here is a difference in our understanding of terminological exactitude (unlike Coolhand Luke whose problem was failure to communicate).

o.k. whatever you say there shaft. not enough time in the day :?


tss