PO-028: Oral transmission of L-type bovine spongiform encephalopathy (L-BSE) in primate model Microcebus murinus
PO-028: Oral transmission of L-type bovine spongiform encephalopathy
(L-BSE) in primate model Microcebus murinus
Nadine Mestre-Frances,1 Simon Nicot,2 Sylvie Rouland,1 Anne-Gaëlle
Biacabe,2 Isabelle Quadrio,3 Armand Perret-Liaudet,3 Thierry Baron,2 Jean-Michel
Verdier1
1IN SER M UM2; Montpellier, France; 2Anses; Lyon, France; 3Hopitaux Civils
de Lyon; Lyon, France
An atypical form of bovine spongiform encephalopathy has been identified in
cattle in Europe, North America and Japan and was designed as L-type BSE (L-BSE)
due to the lower apparent molecular mass of the unglycosylated,
protease-resistant prion protein (PrPres) detected by western blot compared with
classical BSE. Experimental evidences from studies in transgenic mice expressing
human PrP and in primate models suggest a higher risk of transmission to humans
of the L-BSE form than for classical BSE agent. However, a major unresolved
issue concerns the potential transmissibility of the L-BSE agent by oral route.
To address this question, we infected mouse lemurs (Microcebus murinus), a
non-human primate model, with L-BSE by intracerebral or oral route.
Four adult lemurs were intracerebrally (IC) inoculated with 5mg of L-BSE
infected brain homogenate of an atypical French BSE case (02-2528). Four young
and four adult animals were fed with 5 mg or 50 mg of infected brain. After
sacrifice, the brain tissues were biochemically and immunocytochemically
investigated for PrPres.
The 4 animals IC inoculated died at 19 and 22 months postinoculation (mpi).
They developed blindness, tremor, abnormal posture, incoordinated movements,
balance loss. Symptoms get worse according to the disease progression, until
severe ataxia. Severe spongiosis was evidenced into the thalamus, the striatum,
the mesencephalon, and the brainstem, whereas into the cortex the vacuolisation
was weaker. Strong deposits of PrPres were detected into the thalamus, the
striatum, and the hippocampus whereas in the cerebral cortex, PrPres was
prominently accumulated in plaques.
The orally inoculated animals showed similar clinical symptoms occurring
between 27 and 34 mpi. Disease was characterized by progressive prostration,
loss of appetite and poor appearance of the fur. Only one adult animal showed
disequilibrium. PrPres was strongly accumulated only in the striatum and
thalamus and weakly into the cortex. No plaques were evidenced. Two animals that
were orally challenged at the age of two years are still alive and healthy 34
months after inoculation. The western blot analysis showed uniform molecular
profiles, irrespective of the route or dose of infection, and included notably a
PrPres form with low apparent molecular mass (~19 kDa) similar to the PrPres in
the original cattle brain. However, the PrPres profile in lemurs was
characterized by a higher proportion of di- and mono-glycosylated species (up to
95% of the total signal) than in the bovine L-BSE inoculum (~80%). In addition,
small amounts of PrPres were detected by western blotting in the spleen of three
animals (one intra-cerebrally inoculated and two fed with 5 mg of cattle
brain).
Here, we demonstrate that the L-BSE agent can be transmitted by oral route
from cattle to young and adult mouse lemurs. In comparison to IC inoculated
animals, orally challenged lemurs were characterized by longer survival periods
as expected with this route of infection.
Friday, May 25, 2012
R-CALF USDA’s New BSE Rule Eliminates Important Protections Needed to
Prevent BSE Spread
Saturday, May 26, 2012
Are USDA assurances on mad cow case 'gross oversimplification'?
SNIP...
What irks many scientists is the USDA’s April 25 statement that the rare
disease is “not generally associated with an animal consuming infected
feed.”
The USDA’s conclusion is a “gross oversimplification,” said Dr. Paul Brown,
one of the world’s experts on this type of disease who retired recently from the
National Institutes of Health. "(The agency) has no foundation on which to base
that statement.”
“We can’t say it’s not feed related,” agreed Dr. Linda Detwiler, an
official with the USDA during the Clinton Administration now at Mississippi
State.
In the May 1 email to me, USDA’s Cole backed off a bit. “No one knows the
origins of atypical cases of BSE,” she said
The argument about feed is critical because if feed is the cause, not a
spontaneous mutation, the California cow could be part of a larger
outbreak.
SNIP...
Sunday, May 27, 2012
CANADA PLANS TO IMPRISON ANYONE SPEAKING ABOUT MAD COW or ANY OTHER DISEASE
OUTBREAK
CENSORSHIP IS A TERRIBLE THING
Sunday, May 27, 2012
GAIN REPORT BSE Case in United States Will Not Affect Trade, States
Canadian Food Inspection Agency
Subject: Bovine Spongiform Encephalopathy; Importation of Bovines and
Bovine Products APHIS-2008-0010-0008 RIN:0579-AC68
Comment from Terry Singeltary Document ID: APHIS-2008-0010-0008 Document
Type: Public Submission This is comment on Proposed Rule: Bovine Spongiform
Encephalopathy; Importation of Bovines and Bovine Products Docket ID:
APHIS-2008-0010 RIN:0579-AC68
Topics: No Topics associated with this document View Document: More
Document Subtype: Public Comment Status: Posted Received Date: March 22 2012, at
12:00 AM Eastern Daylight Time Date Posted: March 22 2012, at 12:00 AM Eastern
Daylight Time Comment Start Date: March 16 2012, at 12:00 AM Eastern Daylight
Time Comment Due Date: May 15 2012, at 11:59 PM Eastern Daylight Time Tracking
Number: 80fdd617 First Name: Terry Middle Name: S. Last Name: Singeltary City:
Bacliff Country: United States State or Province: TX Organization Name: CJD TSE
PRION Submitter's Representative: CONSUMERS
Comment: comment submission Document ID APHIS-2008-0010-0001
Greetings USDA,
OIE et al, what a difference it makes with science, from one day to the
next. i.e. that mad cow gold card the USA once held. up until that fateful day
in December of 2003, the science of BSE was NO IMPORTS TO USA FROM BSE COUNTRY.
what a difference a day makes$ now that the shoe is on the other foot, the USDA
via the OIE, wants to change science again, just for trade $ I implore the OIE
decision and policy makers, for the sake of the world, to refuse any status quo
of the USA BSE risk assessment. if at al, the USA BSE GBR should be raise to BSE
GBR IV, for the following reasons. North America is awash with many different
TSE Prion strains, in many different species, and they are mutating and
spreading. IF the OIE, and whatever policy makers, do anything but raise the
risk factor for BSE in North America, they I would regard that to be highly
suspicious. IN fact, it would be criminal in my opinion, because the OIE knows
this, and to knowingly expose the rest of the world to this dangerous pathogen,
would be ‘knowingly’ and ‘willfully’, just for the almighty dollar, once again.
I warned the OIE about all this, including the risk factors for CWD, and the
fact that the zoonosis potential was great, way back in 2002. THE OIE in
collaboration with the USDA, made the legal trading of the atypical Nor-98
Scrapie a legal global commodity. yes, thanks to the OIE and the USDA et al,
it’s now legal to trade the atypical Nor-98 Scrapie strain all around the globe.
IF you let them, they will do the same thing with atypical BSE and CWD (both
strains to date). This with science showing that indeed these TSE prion strains
are transmissible. I strenuously urge the OIE et al to refuse any weakening to
the USA trade protocols for the BSE TSE prion disease (all strains), and urge
them to reclassify the USA with BSE GBR IV risk factor.
SEE REFERENCE SOURCES IN ATTACHMENTS
PLEASE SEE Terry S. Singeltary Sr. _Attachment_ WORD FILE ;
***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
snip...
MAD COW USDA ATYPICAL L-TYPE BASE BSE, the rest of the story...
***Oral Transmission of L-type Bovine Spongiform Encephalopathy in Primate
Model
***Infectivity in skeletal muscle of BASE-infected cattle
***feedstuffs- It also suggests a similar cause or source for atypical BSE
in these countries.
***Also, a link is suspected between atypical BSE and some apparently
sporadic cases of Creutzfeldt-Jakob disease in humans.
The present study demonstrated successful intraspecies transmission of
H-type BSE to cattle and the distribution and immunolabeling patterns of PrPSc
in the brain of the H-type BSE-challenged cattle. TSE agent virulence can be
minimally defined by oral transmission of different TSE agents (C-type, L-type,
and H-type BSE agents) [59]. Oral transmission studies with H-type BSEinfected
cattle have been initiated and are underway to provide information regarding the
extent of similarity in the immunohistochemical and molecular features before
and after transmission.
In addition, the present data will support risk assessments in some
peripheral tissues derived from cattle affected with H-type BSE.
in the url that follows, I have posted
SRM breaches first, as late as 2011.
then
MAD COW FEED BAN BREACHES AND TONNAGES OF MAD COW FEED IN COMMERCE up until
2007, when they ceased posting them.
then,
MAD COW SURVEILLANCE BREACHES.
Friday, May 18, 2012
Update from APHIS Regarding a Detection of Bovine Spongiform Encephalopathy
(BSE) in the United States Friday May 18, 2012
TSS
posted by Terry S. Singeltary Sr. at
12:33 PM
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