High Susceptibility Of A Primate Species To The Base Tse [Archive]

flatfish

02-16-2007, 03:17 PM

However, Phillips did not have an explanation of how the first cow got BSE and other

explanations continue to be put forward. One journalist commented on the idea favoured

by the Phillips Committee that BSE started with a spontaneous mutation:

However, apart from there being little evidence for the idea, a random mutation

could not explain why Britain alone has suffered the problem. America, for

instance, has 10 times the number of cattle, and so must in theory run ten times

the risk of a similar random event leading to BSE and so being passed on in

recycled meat and bone meal.13

http://www.parliament.uk/commons/lib/research/rp2001/rp01-089.pdf

Evaluation of the Potential for Bovine Spongiform

Encephalopathy in the United States

Joshua T. Cohen

Keith Duggar

George M. Gray

Silvia Kreindel

Harvard Center for Risk Analysis

Harvard School of Public Health

Hatim Abdelrahman

Tsegaye HabteMariam

David Oryang

Berhanu Tameru

Center for Computational Epidemiology

College of Veterinary Medicine

Tuskegee University

November 26, 2001

snip...

2.3.1 Spontaneous BSE

A potential way in which BSE could be introduced into the United States is the

development of a spontaneous case of a BSE in a native animal. A “spontaneous case” is one that

occurs in an animal with no known risk factors for development of BSE. The presumed

mechanism by which a BSE could occur spontaneously is by the mutation of the PrP gene to a

Section 2

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form that codes for PrPsc, and subsequent recruitment of PrPc until disease is manifest (Prusiner,

1989); (for review see: (Chesebro, 1999). There is no direct evidence of this mechanism,

although some argue that all mammals might have a low spontaneous rate of TSE (Hueston,

1997). In addition, a transgenic animal over-expressing the PrP gene has apparently replicated

the human TSE GSS (Hsiao et al., 1991). Recent results, in which mice expressing the same

point mutation but at normal levels failed to develop disease (Manson et al., 1999), suggest the

mutations may increase susceptibility rather than directly cause the disease. Although at this time

there is no scientific evidence suggesting that spontaneous BSE exists, the BSE Inquiry suggested

that TSEs could possibly develop sporadically in other species, as they do in humans (BSE

Inquiry, 2000). In contrast, the Review of the origin of BSE (Horn et al., 2001) concluded that

although the spontaneous case hypothesis cannot be excluded, there is no evidence supporting the

presence of sporadic form prion disease in cattle or sheep.

snip...

http://www.aphis.usda.gov/lpa/issues/bse/risk_assessment/mainreporttext.pdf

http://www.aphis.usda.gov/lpa/issues/bse/madcow.pdf

WHY is it so difficult to understand that BASE will probably transmit via the oral route via feed as well as with BSE ???

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

TSS