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From: TSS ()
Subject: Prion biology relevant to bovine spongiform encephalopathy1
Date: May 18, 2005 at 1:36 pm PST

-------- Original Message --------
Subject: Prion biology relevant to bovine spongiform encephalopathy1
Date: Tue, 17 May 2005 13:42:29 -0500
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy
To: BSE-L@aegee.org


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

J. Anim. Sci. 2005. 83:1455-1476
© 2005 American Society of Animal Science

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


SPECIAL TOPICS


Prion biology relevant to bovine spongiform encephalopathy1

J. Novakofski*,2, M. S. Brewer{dagger} , N. Mateus-Pinilla{ddagger} , J.
Killefer* and R. H. McCusker*

* Departments of Animal Sciences and {dagger} Food Science and Human
Nutrition, University of Illinois at Urbana–Champaign 61801-4737; and
{ddagger} Illinois Natural History Survey, Center for Wildlife and Plant
Ecology, Champaign, IL 61820

2 Correspondence: 1503 South Maryland Dr. (phone: 217-333-6181; e-mail:
Jnova@uiuc.edu ).

Bovine spongiform encephalopathy (BSE) and chronic wasting disease (CWD)
of deer and elk are a threat to agriculture and natural resources, as
well as a human health concern. Both diseases are transmissible
spongiform encephalopathies (TSE), or prion diseases, caused by
autocatalytic conversion of endogenously encoded prion protein (PrP) to
an abnormal, neurotoxic conformation designated PrPsc. Most mammalian
species are susceptible to TSE, which, despite a range of species-linked
names, is caused by a single highly conserved protein, with no apparent
normal function. In the simplest sense, TSE transmission can occur
because PrPsc is resistant to both endogenous and environmental
proteinases, although many details remain unclear. Questions about the
transmission of TSE are central to practical issues such as livestock
testing, access to international livestock markets, and wildlife
management strategies, as well as intangible issues such as consumer
confidence in the safety of the meat supply. The majority of BSE cases
seem to have been transmitted by feed containing meat and bone meal from
infected animals. In the United Kingdom, there was a dramatic decrease
in BSE cases after neural tissue and, later, all ruminant tissues were
banned from ruminant feed. However, probably because of heightened
awareness and widespread testing, there is growing evidence that new
variants of BSE are arising "spontaneously," suggesting ongoing
surveillance will continue to find infected animals. Interspecies
transmission is inefficient and depends on exposure, sequence homology,
TSE donor strain, genetic polymorphism of the host, and architecture of
the visceral nerves if exposure is by an oral route. Considering the low
probability of interspecies transmission, the low efficiency of oral
transmission, and the low prion levels in nonnervous tissues,
consumption of conventional animal products represents minimal risk.
However, detection of rare events is challenging, and TSE literature is
characterized by subsequently unsupported claims of species barriers or
absolute tissue safety. This review presents an overview of TSE and
summarizes recent research on pathogenesis and transmission.

Key Words: Bovine Spongiform Encephalopathy • Chronic Wasting Disease
• Prion


http://jas.fass.org/cgi/content/abstract/83/6/1455

> there is growing evidence that new variants of BSE are arising
> "spontaneously,"

there is NO evidence of a 'spontaneous' TSE anywhere that
is infectious and shows the pathology of any natural TSE.
if i have missed something, could someone please site this
science to me please.

> Considering the low probability of interspecies transmission, the low
> efficiency of oral transmission, and the low prion levels in
> nonnervous tissues, consumption of conventional animal products
> represents minimal risk.

i disagree with all of the above. all one has to do is read transmission
studies. scrapie infected sheep and goats, CWD infected deer and
elk (who knows how many strains) and undocumented TSEs in the
USA bovine have been rendered and fed to animals for humna/animal
consumption for decades. it's only a pipe dream that none of this
was infectious. to think of a 'spontaneous' TSE as just popping
up from nowhere, is like believing in Santa Claus. remember
the USA scrapie research in Mission, Texas. IT did NOT look
like BSE...

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


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

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

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

PMID: 6997404

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

Oral transmission and early lymphoid tropism of chronic wasting disease
PrPres in mule deer fawns (Odocoileus hemionus )
Christina J. Sigurdson1, Elizabeth S. Williams2, Michael W. Miller3,
Terry R. Spraker1,4, Katherine I. O'Rourke5 and Edward A. Hoover1

Department of Pathology, College of Veterinary Medicine and Biomedical
Sciences, Colorado State University, Fort Collins, CO 80523- 1671, USA1
Department of Veterinary Sciences, University of Wyoming, 1174 Snowy
Range Road, University of Wyoming, Laramie, WY 82070, USA 2
Colorado Division of Wildlife, Wildlife Research Center, 317 West
Prospect Road, Fort Collins, CO 80526-2097, USA3
Colorado State University Veterinary Diagnostic Laboratory, 300 West
Drake Road, Fort Collins, CO 80523-1671, USA4
Animal Disease Research Unit, Agricultural Research Service, US
Department of Agriculture, 337 Bustad Hall, Washington State University,
Pullman, WA 99164-7030, USA5

Author for correspondence: Edward Hoover.Fax +1 970 491 0523. e-mail
ehoover@lamar.colostate.edu

Mule deer fawns (Odocoileus hemionus) were inoculated orally with a
brain homogenate prepared from mule deer with naturally occurring
chronic wasting disease (CWD), a prion-induced transmissible spongiform
encephalopathy. Fawns were necropsied and examined for PrP res, the
abnormal prion protein isoform, at 10, 42, 53, 77, 78 and 80 days
post-inoculation (p.i.) using an immunohistochemistry assay modified to
enhance sensitivity. PrPres was detected in alimentary-tract-associated
lymphoid tissues (one or more of the following: retropharyngeal lymph
node, tonsil, Peyer's patch and ileocaecal lymph node) as early as 42
days p.i. and in all fawns examined thereafter (53 to 80 days p.i.). No
PrPres staining was detected in lymphoid tissue of three control fawns
receiving a control brain inoculum, nor was PrPres detectable in neural
tissue of any fawn. PrPres-specific staining was markedly enhanced by
sequential tissue treatment with formic acid, proteinase K and hydrated
autoclaving prior to immunohistochemical staining with monoclonal
antibody F89/160.1.5. These results indicate that CWD PrP res can be
detected in lymphoid tissues draining the alimentary tract within a few
weeks after oral exposure to infectious prions and may reflect the
initial pathway of CWD infection in deer. The rapid infection of deer
fawns following exposure by the most plausible natural route is
consistent with the efficient horizontal transmission of CWD in nature
and enables accelerated studies of transmission and pathogenesis in the
native species.

snip...

These results indicate that mule deer fawns develop detectable PrP res
after oral exposure to an inoculum containing CWD prions. In the
earliest post-exposure period, CWD PrPres was traced to the lymphoid
tissues draining the oral and intestinal mucosa (i.e. the
retropharyngeal lymph nodes, tonsil, ileal Peyer's patches and
ileocaecal lymph nodes), which probably received the highest initial
exposure to the inoculum. Hadlow et al. (1982) demonstrated scrapie
agent in the tonsil, retropharyngeal and mesenteric lymph nodes, ileum
and spleen in a 10-month-old naturally infected lamb by mouse bioassay.
Eight of nine sheep had infectivity in the retropharyngeal lymph node.
He concluded that the tissue distribution suggested primary infection
via the gastrointestinal tract. The tissue distribution of PrPres in the
early stages of infection in the fawns is strikingly similar to that
seen in naturally infected sheep with scrapie. These findings support
oral exposure as a natural route of CWD infection in deer and support
oral inoculation as a reasonable exposure route for experimental studies
of CWD.

snip...

http://vir.sgmjournals.org/cgi/content/full/80/10/2757

3. You will recall that the advice provided by Professor Smith in
1993 and by Dr. Gore this month used the sub-population of dairy
farm workers who had had a case of BSE on their farms -
63,000, which is approximately half the number of dairy farm
workers - as a denominator. If the above sums are repeated using
this denominator population, taking an annual incidence in the general
population of 1 per million the observed rate in this sub-population
is 10 TIMES, and taking an annual incidence of 0.7 per million,
IT IS 15 TIMES (THE ''WORST CASE'' SCENARIO) than
that in the general population...

http://www.bseinquiry.gov.uk/files/yb/1995/01/31004001.pdf


It was, however, performed in the USA in 1979, when it was shown that
cattle inoculated with the scrapie agent endemic in the flock of Suffolk
sheep at the United States Department of Agriculture in Mission, Texas,
developed a TSE quite unlike BSE. 32 <

http://www.bseinquiry.gov.uk/report/volume2/chaptea3.htm#820543

The findings of the initial transmission, though not of the clinical or
neurohistological examination, were communicated in October 1988 to Dr
Watson, Director of the CVL, following a visit by Dr Wrathall, one of
the project leaders in the Pathology Department of the CVL, to the
United States Department of Agriculture. 33


http://www.bseinquiry.gov.uk/report/volume2/chaptea3.htm#820546


The results were not published at this point, since the attempted
transmission to mice from the experimental cow brain had been
inconclusive. The results of the clinical and histological differences
between scrapie-affected sheep and cattle were published in 1995.
Similar studies in which cattle were inoculated intracerebrally with
scrapie inocula derived from a number of scrapie-affected sheep of
different breeds and from different States, were carried out at the US
National Animal Disease Centre. 34


http://www.bseinquiry.gov.uk/report/volume2/chaptea3.htm#820549


The results, published in 1994, showed that this source of scrapie
agent, though pathogenic for cattle, did not produce the same clinical
signs of brain lesions characteristic of BSE.


http://www.bseinquiry.gov.uk/report/volume2/chaptea3.htm


Visit to USA ... info on BSE and Scrapie


http://www.bseinquiry.gov.uk/files/yb/1988/10/00001001.pdf


HOUND STUDY

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

snip...

http://www.bseinquiry.gov.uk/files/yb/1991/01/04004001.pdf


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


http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf

WHY is USA insisting _now_ not to use WB, when on the 1st _confirmed_
case Dec. 23, 2003
USA mad cow, WB was used ???

maybe this is the reason ;

JAPAN BSE # 8 & 9 cow

8. 6/10/2003 Holstein Steer 13/10/2001 23 mths
No clinical signs WB+, IHC-, HP-


9. 4/11/2003 Holstein Steer 13/1/2002
21 mths No clinical signs WB+, IHC-, HP-

===========

More information on the first 11 Japanese BSE-cases can be found on the
website of the Japanese Embassy in the US:

http://www.us.emb-japan.go.jp/english/html/fafacts/bse/bse.htm

IN fact, the new strain of TSE in cattle BaSE, does not look like nvCJD
in humans, but very similar
to the sporadic CJD;


BASE in cattle in Italy of Identification of a second bovine amyloidotic
spongiform encephalopathy: Molecular similarities with sporadic
Creutzfeldt-Jakob disease

http://www.pnas.org/cgi/content/abstract/0305777101v1


Adaptation of the bovine spongiform encephalopathy agent to primates and
comparison with Creutzfeldt- Jakob disease: Implications for human
health THE findings from Corinne Ida Lasmézas*, [dagger] , Jean-Guy
Fournier*, Virginie Nouvel*, Hermann Boe*, Domíníque Marcé*,
François Lamoury*, Nicolas Kopp [Dagger ] , Jean-Jacques Hauw§, James
Ironside¶, Moira Bruce [||] , Dominique Dormont*, and Jean-Philippe
Deslys* et al, that The agent responsible for French iatrogenic growth
hormone-linked CJD taken as a control is very different from vCJD but is
similar to that found in one case of sporadic CJD and one sheep scrapie
isolate;


http://www.pnas.org/cgi/content/full/041490898v1


Characterization of two distinct prion strains derived from bovine
spongiform encephalopathy transmissions to inbred mice


http://vir.sgmjournals.org/cgi/content/abstract/85/8/2471


USA BSE GBR III

http://www.efsa.eu.int/science/efsa_scientific_reports/gbr_assessments/scr_annexes/574/sr03_biohaz02_usa_report_annex_en1.pdf


http://www.fda.gov/ohrms/dockets/dockets/03n0312/03N-0312_emc-000001.txt

https://web01.aphis.usda.gov/regpublic.nsf/0/eff9eff1f7c5cf2b87256ecf000df08d?OpenDocument


https://web01.aphis.usda.gov/BSEcom.nsf/0/b78ba677e2b0c12185256dd300649f9d?OpenDocument&AutoFramed


TSS

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