National Scrapie Eradication Program November 2014 Monthly Report Fiscal
U.S. Department of Agriculture
Animal and Plant Health Inspection Service
Surveillance, Response and Preparedness Services
Sheep and Goat Health Program
December 15, 2014
INTRODUCTION - Program Summary
At the end of FY 2014, the percent of cull black face sheep found positive
at slaughter was 0.02 percent (Chart 1). This measure decreased by 51 percent
compared to FY 2013 and 98 percent compared to FY 2003. Eight source flocks
(including 2 goat herds) and 3 infected flocks were designated in FY 2013. Three
source flocks and 3 infected flocks were designated in FY 2014 (Chart 2), a
decrease of 45 percent. One source flock has been designated in FY 2015.
At the end of FY 2014, the percent of cull sheep found positive at
slaughter and adjusted for face color* was 0.019 percent (Chart 3). This measure
increased by 31 percent compared to FY 2013 and decreased 87 percent compared to
* See slide 4 for an explanation of adjusted weights.
Introduction - Program Summary
INTRODUCTION - Surveillance (Part 1)
Regulatory Scrapie Slaughter Surveillance (RSSS)
RSSS started April 1, 2003. It is a targeted slaughter surveillance program
which is designed to identify infected flocks. Samples have been collected from
451,240 animals since April 1, 2003. There have been 475 NVSL confirmed positive
animals* (467 classical cases and 8 Nor98-like cases) since the beginning of
RSSS. As of November 30, 2014, 7,502 samples have been collected in FY 2015,
6,010 from sheep and 1,492 from goats.
As of November 30, 2014, 1 goat has tested positive for scrapie; this is
the first positive goat case found through RSSS. The weighted percentage of
samples from sheep that have tested positive for each face color from FY 2003
through FY 2015 is depicted in Chart 3. In November 2013, administrative units
within APHIS Veterinary Services reorganized from 2 Regions to 6 Districts
(Figure 1). The distribution of sheep and goat populations by District is
depicted in Chart 4a. The number of animals collected for FY 2015 by District
where collected is shown in Chart 4b. A monthly comparison of RSSS collections
by fiscal year is displayed in Chart 5. Chart 6 is a retrospective 6-month
rolling average of the percent positive, black-faced sheep sampled at RSSS
* RSSS positives are reported based on collection date and may have been
confirmed after November 30, 2014.
** White, black and mottled face color sheep are weighted based on
population. White faced sheep have the highest weight, so when the uncommon
white face positive sheep is found it will cause this statistic to increase.
Goats and other face colored sheep are not included in this calculation.
Introduction – Surveillance (Part 1)
Introduction – Surveillance (Part 1)
INTRODUCTION - Surveillance (Part 2) On-Farm Surveillance Testing sheep and
goats on-farm is an essential part of scrapie surveillance. It includes both
regulatory testing of scrapie exposed and potentially exposed sheep and goats
and testing sheep and goats on farm for routine surveillance. As the National
Scrapie Eradication Program moves closer towards meeting the goal of identifying
the last remaining cases of classical scrapie, finding and testing all sheep and
goats meeting targeted sampling criteria is even more important. As of November
30, 2014, 217 sheep and 105 goats have been tested on-farm for FY 2015. One
clinical suspect sheep and two other sheep from the same flock have tested
positive. The number of animals tested on-farm by month and by species for FY
2015 is shown in Chart 7. Total Animals Sampled for Scrapie Testing As of
November 30, 2014, 7,824 animals have been sampled for scrapie testing in FY
• 7,502 RSSS samples and 322 on-farm samples (Chart 8);
• Of which 6,227 were sheep and 1,597 were goats. Distribution of sampling
by type (RSSS or on-farm) and by species is shown in Chart 9.
INTRODUCTION - Positive Cases and Infected/Source Flocks
Positive Scrapie Cases*
Through On-Farm surveillance, one clinical suspect sheep tested positive
for scrapie in November. (Table 7 and Figure 2). The flock of origin was
designated as a source flock. Since the designation, two other sheep from the
flock died and tested positive for scrapie.
The first RSSS positive goat was reported in November 2014. This case
increases the number of confirmed positive cases in goats since FY 2002 to 40
(Table 7 and Figure 3). Infected and Source Flocks
As of November 30, 2014, there were 5 flocks with an open infected or
(Figure 4). One new source flock has been designated in FY 2015. (Figure
5). New infected and source statuses from FY 1997 to FY 2015 are depicted in
* Samples collected between October 1, 2014 and November 30, 2014 and
confirmed by December 15, 2014. Cases and New Infected/Source Flocks
INTRODUCTION - Scrapie Flock Certification Program (SFCP)
As of November 30, 2014, there were 453 flocks participating in the Scrapie
Flock Certification Program (SFCP). Statuses of these flocks were 178 export
monitored, 18 export certified, and 257 select monitored flocks (Figure 6). SFCP
open statuses by fiscal year from FY 2007 to FY 2015 are depicted in Chart
The current status of participating flocks is available to the public on
the SFCP Web Page.1
The current version of the SFCP standards was published June 20, 2013. A
copy of the standards can be downloaded from APHIS’ SFCP Web Page.
1 Note: Flocks that have “Certified” status on the SFCP Web Page are not
listed in this report because it is a transitional status concurrent with their
Export Monitored status.
This report is based on information and test results available at the time
of report generation. Numbers are subject to change due to later reporting of
test results and updates in the database.
snip...see full text ;
Tuesday, December 16, 2014
Evidence for zoonotic potential of ovine scrapie prions
Hervé Cassard,1, n1 Juan-Maria Torres,2, n1 Caroline Lacroux,1, Jean-Yves
Douet,1, Sylvie L. Benestad,3, Frédéric Lantier,4, Séverine Lugan,1, Isabelle
Lantier,4, Pierrette Costes,1, Naima Aron,1, Fabienne Reine,5, Laetitia
Herzog,5, Juan-Carlos Espinosa,2, Vincent Beringue5, & Olivier Andréoletti1,
Affiliations Contributions Corresponding author Journal name: Nature
Communications Volume: 5, Article number: 5821 DOI: doi:10.1038/ncomms6821
Received 07 August 2014 Accepted 10 November 2014 Published 16 December 2014
Article tools Citation Reprints Rights & permissions Article metrics
Although Bovine Spongiform Encephalopathy (BSE) is the cause of variant
Creutzfeldt Jakob disease (vCJD) in humans, the zoonotic potential of scrapie
prions remains unknown. Mice genetically engineered to overexpress the human
prion protein (tgHu) have emerged as highly relevant models for gauging the
capacity of prions to transmit to humans. These models can propagate human
prions without any apparent transmission barrier and have been used used to
confirm the zoonotic ability of BSE. Here we show that a panel of sheep scrapie
prions transmit to several tgHu mice models with an efficiency comparable to
that of cattle BSE. The serial transmission of different scrapie isolates in
these mice led to the propagation of prions that are phenotypically identical to
those causing sporadic CJD (sCJD) in humans. These results demonstrate that
scrapie prions have a zoonotic potential and raise new questions about the
possible link between animal and human prions.
Subject terms: Biological sciences• Medical research At a glance
why do we not want to do TSE transmission studies on chimpanzees $
5. A positive result from a chimpanzee challenged severly would likely
create alarm in some circles even if the result could not be interpreted for
man. I have a view that all these agents could be transmitted provided a large
enough dose by appropriate routes was given and the animals kept long enough.
Until the mechanisms of the species barrier are more clearly understood it might
be best to retain that hypothesis.
1: J Infect Dis 1980 Aug;142(2):205-8
Oral transmission of kuru, Creutzfeldt-Jakob disease, and scrapie to
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
The successful transmission of kuru, Creutzfeldt-Jakob disease, and scrapie
by natural feeding to squirrel monkeys that we have reported provides further
grounds for concern that scrapie-infected meat may occasionally give rise in
humans to Creutzfeldt-Jakob disease.
Recently the question has again been brought up as to whether scrapie is
transmissible to man. This has followed reports that the disease has been
transmitted to primates. One particularly lurid speculation (Gajdusek 1977)
conjectures that the agents of scrapie, kuru, Creutzfeldt-Jakob disease and
transmissible encephalopathy of mink are varieties of a single "virus". The U.S.
Department of Agriculture concluded that it could "no longer justify or permit
scrapie-blood line and scrapie-exposed sheep and goats to be processed for human
or animal food at slaughter or rendering plants" (ARC 84/77)" The problem is
emphasised by the finding that some strains of scrapie produce lesions identical
to the once which characterise the human dementias"
Whether true or not. the hypothesis that these agents might be
transmissible to man raises two considerations. First, the safety of laboratory
personnel requires prompt attention. Second, action such as the "scorched meat"
policy of USDA makes the solution of the acrapie problem urgent if the sheep
industry is not to suffer grievously.
Nature. 1972 Mar 10;236(5341):73-4.
Transmission of scrapie to the cynomolgus monkey (Macaca fascicularis).
Gibbs CJ Jr, Gajdusek DC.
Nature 236, 73 - 74 (10 March 1972); doi:10.1038/236073a0
Transmission of Scrapie to the Cynomolgus Monkey (Macaca fascicularis)
C. J. GIBBS jun. & D. C. GAJDUSEK
National Institute of Neurological Diseases and Stroke, National Institutes
of Health, Bethesda, Maryland
SCRAPIE has been transmitted to the cynomolgus, or crab-eating, monkey
(Macaca fascicularis) with an incubation period of more than 5 yr from the time
of intracerebral inoculation of scrapie-infected mouse brain. The animal
developed a chronic central nervous system degeneration, with ataxia, tremor and
myoclonus with associated severe scrapie-like pathology of intensive astroglial
hypertrophy and proliferation, neuronal vacuolation and status spongiosus of
grey matter. The strain of scrapie virus used was the eighth passage in Swiss
mice (NIH) of a Compton strain of scrapie obtained as ninth intracerebral
passage of the agent in goat brain, from Dr R. L. Chandler (ARC, Compton,
What if you can catch old-fashioned CJD by eating meat from a sheep
infected with scrapie?
28 Mar 01
Like lambs to the slaughter
31 March 2001
by Debora MacKenzie Magazine issue 2284.
FOUR years ago, Terry Singeltary watched his mother die horribly from a
degenerative brain disease. Doctors told him it was Alzheimer's, but Singeltary
was suspicious. The diagnosis didn't fit her violent symptoms, and he demanded
an autopsy. It showed she had died of sporadic Creutzfeldt-Jakob disease.
Most doctors believe that sCJD is caused by a prion protein deforming by
chance into a killer. But Singeltary thinks otherwise. He is one of a number of
campaigners who say that some sCJD, like the variant CJD related to BSE, is
caused by eating meat from infected animals. Their suspicions have focused on
sheep carrying scrapie, a BSE-like disease that is widespread in flocks across
Europe and North America.
Now scientists in France have stumbled across new evidence that adds weight
to the campaigners' fears. To their complete surprise, the researchers found
that one strain of scrapie causes the same brain damage in mice as sCJD.
"This means we cannot rule out that at least some sCJD may be caused by
some strains of scrapie," says team member Jean-Philippe Deslys of the French
Atomic Energy Commission's medical research laboratory in Fontenay-aux-Roses,
south-west of Paris. Hans Kretschmar of the University of Göttingen, who
coordinates CJD surveillance in Germany, is so concerned by the findings that he
now wants to trawl back through past sCJD cases to see if any might have been
caused by eating infected mutton or lamb.
Scrapie has been around for centuries and until now there has been no
evidence that it poses a risk to human health. But if the French finding means
that scrapie can cause sCJD in people, countries around the world may have
overlooked a CJD crisis to rival that caused by BSE.
Deslys and colleagues were originally studying vCJD, not sCJD. They
injected the brains of macaque monkeys with brain from BSE cattle, and from
French and British vCJD patients. The brain damage and clinical symptoms in the
monkeys were the same for all three. Mice injected with the original sets of
brain tissue or with infected monkey brain also developed the same
As a control experiment, the team also injected mice with brain tissue from
people and animals with other prion diseases: a French case of sCJD; a French
patient who caught sCJD from human-derived growth hormone; sheep with a French
strain of scrapie; and mice carrying a prion derived from an American scrapie
strain. As expected, they all affected the brain in a different way from BSE and
vCJD. But while the American strain of scrapie caused different damage from
sCJD, the French strain produced exactly the same pathology.
"The main evidence that scrapie does not affect humans has been
epidemiology," says Moira Bruce of the neuropathogenesis unit of the Institute
for Animal Health in Edinburgh, who was a member of the same team as Deslys.
"You see about the same incidence of the disease everywhere, whether or not
there are many sheep, and in countries such as New Zealand with no scrapie." In
the only previous comparisons of sCJD and scrapie in mice, Bruce found they were
But there are more than 20 strains of scrapie, and six of sCJD. "You would
not necessarily see a relationship between the two with epidemiology if only
some strains affect only some people," says Deslys. Bruce is cautious about the
mouse results, but agrees they require further investigation. Other trials of
scrapie and sCJD in mice, she says, are in progress.
People can have three different genetic variations of the human prion
protein, and each type of protein can fold up two different ways. Kretschmar has
found that these six combinations correspond to six clinical types of sCJD: each
type of normal prion produces a particular pathology when it spontaneously
deforms to produce sCJD.
But if these proteins deform because of infection with a disease-causing
prion, the relationship between pathology and prion type should be different, as
it is in vCJD. "If we look at brain samples from sporadic CJD cases and find
some that do not fit the pattern," says Kretschmar, "that could mean they were
caused by infection."
There are 250 deaths per year from sCJD in the US, and a similar incidence
elsewhere. Singeltary and other US activists think that some of these people
died after eating contaminated meat or "nutritional" pills containing dried
animal brain. Governments will have a hard time facing activists like Singeltary
if it turns out that some sCJD isn't as spontaneous as doctors have
Deslys's work on macaques also provides further proof that the human
disease vCJD is caused by BSE. And the experiments showed that vCJD is much more
virulent to primates than BSE, even when injected into the bloodstream rather
than the brain. This, says Deslys, means that there is an even bigger risk than
we thought that vCJD can be passed from one patient to another through
contaminated blood transfusions and surgical instruments.
Tuesday, December 23, 2014
*** FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED
VIOLATIONS OFFICIAL ACTION INDICATED OAI UPDATE DECEMBER 2014 BSE TSE PRION
Sunday, December 21, 2014
*** Mucosal immunization with an attenuated Salmonella vaccine partially
protects white-tailed deer from chronic wasting disease
CWD TO HUMANS, AND RISK FACTORS THERE FROM (see latest science)
Tuesday, November 04, 2014
*** Six-year follow-up of a point-source exposure to CWD contaminated
venison in an Upstate New York community: risk behaviours and health outcomes
Friday, December 5, 2014
*** SPECIAL ALERT The OIE recommends strengthening animal disease
surveillance worldwide OIE
BSE TSE PRION AKA MAD COW DISEASE ? ‘’the silence was deafening’’ ...tss
*** HUMAN MAD COW DISEASE nvCJD TEXAS CASE NOT LINKED TO EUROPEAN TRAVEL
Sunday, November 23, 2014
*** Confirmed Variant Creutzfeldt-Jakob Disease (variant CJD) Case in Texas
in June 2014 confirmed as USA case NOT European
the patient had resided in Kuwait, Russia and Lebanon. The completed
investigation did not support the patient's having had extended travel to
European countries, including the United Kingdom, or travel to Saudi Arabia. The
specific overseas country where this patient’s infection occurred is less clear
largely because the investigation did not definitely link him to a country where
other known vCJD cases likely had been infected.
Sunday, December 14, 2014
*** ALERT new variant Creutzfeldt Jakob Disease nvCJD or vCJD, sporadic CJD
strains, TSE prion aka Mad Cow Disease United States of America Update December
14, 2014 Report