Chronic Wasting Disease Q&A from St. Joseph MO MDC meeting 9/30/13 TSS COMMENTS
Chronic Wasting Disease Q&A from St. Joseph MO MDC meeting TSS COMMENTS
Greetings Missouri Wildlife officials and government officials,
I kindly wish to comment on the following please ;
Chronic Wasting Disease Q&A from St. Joseph MO MDC meeting
Chronic Wasting Disease Q&A from St. Joseph MO MDC meeting claimed ;
>>> NO THREAT TO CATTLE HERDS ?
>>> COMMINGLING OF CWD cervids WITH CATTLE NO RISK???
>>> cwd to humans, no risk ???
>>>cwd no risk factor from the world of insects
THAT IS not exactly correct. same as the assumption that cwd will not
affect humans. true, no documented cases to date, of cwd transmission to cattle,
or humans. but please let me give you a few factors to a few of these
assumptions.
first off, the surveillance for human TSE from the many different animal
TSE prion disease here in North America, and any iatrogenic event there from, is
seriously flawed, and TSEs such as atypical BSE strains, or the different CWD
strains, to humans, will not look like nvCJD, of which the nvCJD cases were
documented mostly in the UK. however, the risk is very real, and science has
shown this. atypical BSE is more virulent than the typical BSE cases, and they
do not know if this different TSE in the bovine, will transmit to the cervids,
or visa versa. also, what about the shedding of the typical and atypical BSE
prions into the environment, and the uptaking there from by cervids? and if you
look and compare cwd with scrapie, and recent transmission studies there from,
for anyone to state that there has been no risk of transmission to humans or
cattle from CWD, or visa versa, especially now that we have more than one strain
of CWD, would be (in my opinion) very foolish. the science is there that shows
these risk factors. every time some think the prion can’t, it proves them wrong.
some of the most famous lines I remember from the past would go like this;
>>>BSE mad cow disease will not affect humans...
IT DID, IT HAS, AND IS STILL AFFECTING THEM.
BSE cannot/will not/has not trasmit to other species;
BSE has transmitted to primate, porcine, fowl, and even big bird, i.e.
red-tailed ostrich, feline, canine, and many, many species in zoo animals from
oral consumption of split carcasses of the bovine, ...and I could go on here,
but science has well documented all this. ...in my opinion, this is NOT rocket
science. what it IS, is the incubation period, and the fact that industrial and
political science has won out over sound peer review science. I remind you all
of asbestos and tobacco. just saying...tss
>>>sporadic CJD is not related to BSE mad cow disease...
SCIENCE HAS NOW SHOWN THAT INDEED SOME SPORADIC CJD CASES ARE LINKED TO
ATYPICAL BSE AND ATYPICAL SCRAPIE.
>>>nvCJD will not transmit by blood...
BLOOD HAS NOW BEEN LINKED TO FOUR nvCJD CASES. ...
>>>mad cow disease is not in the USA, our triple mad cow firewall
will protect us from any mad cow disease...
THERE NOW HAS BEEN TYPICAL C-BSE, ATYPICAL BASE L-TYPE BSE, ATYPICAL H-TYPE
BSE, AND ATYPICAL Hg-type BSE DOCUMENTED IN NORTH AMERICA AND THE USA.
P.4.23
Transmission of atypical BSE in humanized mouse models
Liuting Qing1, Wenquan Zou1, Cristina Casalone2, Martin Groschup3, Miroslaw
Polak4, Maria Caramelli2, Pierluigi Gambetti1, Juergen Richt5, Qingzhong Kong1
1Case Western Reserve University, USA; 2Instituto Zooprofilattico Sperimentale,
Italy; 3Friedrich-Loeffler-Institut, Germany; 4National Veterinary Research
Institute, Poland; 5Kansas State University (Previously at USDA National Animal
Disease Center), USA
Background: Classical BSE is a world-wide prion disease in cattle, and the
classical BSE strain (BSE-C) has led to over 200 cases of clinical human
infection (variant CJD). Atypical BSE cases have been discovered in three
continents since 2004; they include the L-type (also named BASE), the H-type,
and the first reported case of naturally occurring BSE with mutated bovine PRNP
(termed BSE-M). The public health risks posed by atypical BSE were largely
undefined.
Objectives: To investigate these atypical BSE types in terms of their
transmissibility and phenotypes in humanized mice. Methods: Transgenic mice
expressing human PrP were inoculated with several classical (C-type) and
atypical (L-, H-, or Mtype) BSE isolates, and the transmission rate, incubation
time, characteristics and distribution of PrPSc, symptoms, and histopathology
were or will be examined and compared.
Results: Sixty percent of BASE-inoculated humanized mice became infected
with minimal spongiosis and an average incubation time of 20-22 months, whereas
only one of the C-type BSE-inoculated mice developed prion disease after more
than 2 years. Protease-resistant PrPSc in BASE-infected humanized Tg mouse
brains was biochemically different from bovine BASE or sCJD. PrPSc was also
detected in the spleen of 22% of BASE-infected humanized mice, but not in those
infected with sCJD. Secondary transmission of BASE in the humanized mice led to
a small reduction in incubation time.*** The atypical BSE-H strain is also
transmissible with distinct phenotypes in the humanized mice, but no BSE-M
transmission has been observed so far.
Discussion: Our results demonstrate that BASE is more virulent than
classical BSE, has a lymphotropic phenotype, and displays a modest transmission
barrier in our humanized mice. BSE-H is also transmissible in our humanized Tg
mice. The possibility of more than two atypical BSE strains will be discussed.
Supported by NINDS NS052319, NIA AG14359, and NIH AI 77774.
Given the quantitative indicators of what seems, in the EU, to be the
near-extinction of the animal epidemic and control of cattle-to-human
transmission, is there anything left for concern? Unfortunately, there is. With
BSE, the global disease burden is far from clear in countries with less
well-developed surveillance. In humans, the potential continuing person to
person spread by blood and blood products remains a problem as seen with the
four cases of transfusion-associated vCJD infection to date (Andrews, 2011).
With BSE and other TSEs in animals, the recognition of the wide diversity of
prion strains in the field, including three new forms of animal TSEs (L-type
Atypical BSE, H-type Atypical BSE and Atypical scrapie), has complicated disease
diagnosis and surveillance, as well as scientific assessment of their potential
risks to humans. EFSA and the European Centre for Disease Prevention and Control
(ECDC) recently delivered a scientific opinion on any possible epidemiological
or molecular association between TSEs in animals and humans (EFSA Panel on
Biological Hazards (BIOHAZ) and ECDC, 2011). This opinion confirmed Classical
BSE prions as the only TSE agents demonstrated to be zoonotic so far but the
possibility that a small proportion of human cases so far classified as
"sporadic" CJD are of zoonotic origin could not be excluded. Moreover,
transmission experiments to non-human primates suggest that some TSE agents in
addition to Classical BSE prions in cattle (namely L-type Atypical BSE,
Classical BSE in sheep, transmissible mink encephalopathy (TME) and chronic
wasting disease (CWD) agents) might have zoonotic potential. In particular the
L-type Atypical BSE agent might be similarly or even more virulent to humans
than the Classical BSE agent. While mankind has been in contact with the major
TSE of small ruminants for centuries, there is no epidemiological evidence to
suggest that classical scrapie is zoonotic; however, experimental transmission
data on humanised mice and non-human primates have been very scarce so
far.
What does this mean for the future? The decline of the BSE epidemic seen by
2005 led to consideration of some relaxation of costly BSE control measures as
depicted in the EU TSE Roadmap (EC, 2005), and will inevitably be followed by
further relaxation as already outlined in another EU TSE Roadmap 2 of 2010 (EC,
2010). It remains critical that current levels of consumer protection are
maintained and all future changes from well established and highly effective
current risk management measures are based upon sound scientific advice that
EFSA will continue to provide.
Which old issues will remain, and which new issues will become relevant?
For Atypical BSE, the most widely accepted hypothesis is that of a spontaneously
arising ("sporadic") disease in relatively old bovines. If this holds true, it
will be impossible to eradicate such a disease which originates de novo;
probably we then have to live forever with a ban on SRMs, in particular the
central nervous system (CNS), of older cattle. Given our insufficient knowledge
about the true prevalence of atypical animal prion strains in the field, it will
be important to continue and improve the systematic surveillance of animal TSEs,
and to refine our diagnostic and laboratory methods and experiments. As some
scientific data suggest that there is probably no absolute molecular barrier to
transmission of TSE agents between mammalian species (EFSA Panel on Biological
Hazards (BIOHAZ) and ECDC, 2011), the issue of a zoonotic potential of prions is
likely to remain with us a time. For human TSEs including sporadic CJD, it will
be important to continue systematic surveillance that should be able, as clearly
shown with vCJD in the past, eventually to identify emerging new phenotypes or
new prion strains. In sum, at a time when many scientists and most decision
makers are no longer interested in prions and their risk, it will be prudent to
stay vigilant, although this must be in a way that is balanced with other risks
to human and animal health. In the risk assessment area, this will continue to
be a challenge for EFSA in the years to come.
--------------------------------------------------------------------------------
[1] Regulation (EC) No 999/2001 of the European Parliament and of the
Council of 22 May 2001 laying down rules for the prevention, control and
eradication of certain transmissible spongiform encephalopathies. OJ L 147,
31.05.2001, p. 1-40.
see full text and more here ;
believing that a strain or certain genotype of one TSE prion disease, is
resistant to any TSE prion disease, EXAMPLE, like the sheep homozygous for the
resistant PrPARR allele (A136R154R171),... efficiently transmitted the disease
to transgenic mice expressing ovine PrP, and that they shared unique biological
and biochemical features upon propagation in mice. These observations support
the view that a truly infectious TSE agent, unrecognized until recently, infects
sheep and goat flocks and may have important implications in terms of scrapie
control and public health. ...never say never with the TSE prion disease...http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1276041/
OR RABBITS, OR CANINE, OR ....SEE LINKS WITH TRANSMISSION STUDIES
BELOW.
never say never with the tse prion disease.
ONE PARTICULAR QUESTION, what about tse from typical bse and or the
atypical bse TSE STRAINS in the environment, and potential shedding there from,
might there be a risk to cervids ?
I think by now we should be aware of the risk factors of sheep scrapie to
cervids via transmission studies ;
pens, pens, PENS ???
*** Spraker suggested an interesting explanation for the occurrence of CWD.
The deer pens at the Foot Hills Campus were built some 30-40 years ago by a Dr.
Bob Davis. At or abut that time, allegedly, some scrapie work was conducted at
this site. When deer were introduced to the pens they occupied ground that had
previously been occupied by sheep.
now, decades later ;
2012
PO-039: A comparison of scrapie and chronic wasting disease in white-tailed
deer
Justin Greenlee, Jodi Smith, Eric Nicholson US Dept. Agriculture;
Agricultural Research Service, National Animal Disease Center; Ames, IA USA
Interspecies transmission studies afford the opportunity to better
understand the potential host range and origins of prion diseases. The purpose
of these experiments was to determine susceptibility of white-tailed deer (WTD)
to scrapie and to compare the resultant clinical signs, lesions, and molecular
profiles of PrPSc to those of chronic wasting disease (CWD). We inoculated WTD
intracranially (IC; n = 5) and by a natural route of exposure (concurrent oral
and intranasal (IN); n = 5) with a US scrapie isolate. All deer were inoculated
with a 10% (wt/vol) brain homogenate from sheep with scrapie (1ml IC, 1 ml IN,
30 ml oral). All deer inoculated by the intracranial route had evidence of PrPSc
accumulation. PrPSc was detected in lymphoid tissues as early as 7
months-post-inoculation (PI) and a single deer that was necropsied at 15.6
months had widespread distribution of PrPSc highlighting that PrPSc is widely
distributed in the CNS and lymphoid tissues prior to the onset of clinical
signs. IC inoculated deer necropsied after 20 months PI (3/5) had clinical
signs, spongiform encephalopathy, and widespread distribution of PrPSc in neural
and lymphoid tissues. The results of this study suggest that there are many
similarities in the manifestation of CWD and scrapie in WTD after IC inoculation
including early and widespread presence of PrPSc in lymphoid tissues, clinical
signs of depression and weight loss progressing to wasting, and an incubation
time of 21-23 months. Moreover, western blots (WB) done on brain material from
the obex region have a molecular profile similar to CWD and distinct from
tissues of the cerebrum or the scrapie inoculum. However, results of microscopic
and IHC examination indicate that there are differences between the lesions
expected in CWD and those that occur in deer with scrapie: amyloid plaques were
not noted in any sections of brain examined from these deer and the pattern of
immunoreactivity by IHC was diffuse rather than plaque-like. After a natural
route of exposure, 100% of WTD were susceptible to scrapie. Deer developed
clinical signs of wasting and mental depression and were necropsied from 28 to
33 months PI. Tissues from these deer were positive for PrPSc by IHC and WB.
Similar to IC inoculated deer, samples from these deer exhibited two different
molecular profiles: samples from obex resembled CWD whereas those from cerebrum
were similar to the original scrapie inoculum. On further examination by WB
using a panel of antibodies, the tissues from deer with scrapie exhibit
properties differing from tissues either from sheep with scrapie or WTD with
CWD. Samples from WTD with CWD or sheep with scrapie are strongly immunoreactive
when probed with mAb P4, however, samples from WTD with scrapie are only weakly
immunoreactive. In contrast, when probed with mAb’s 6H4 or SAF 84, samples from
sheep with scrapie and WTD with CWD are weakly immunoreactive and samples from
WTD with scrapie are strongly positive. This work demonstrates that WTD are
highly susceptible to sheep scrapie, but on first passage, scrapie in WTD is
differentiable from CWD.
2011
*** After a natural route of exposure, 100% of white-tailed deer were
susceptible to scrapie.
Scrapie in Deer: Comparisons and Contrasts to Chronic Wasting Disease (CWD)
Justin J. Greenlee of the Virus and Prion Diseases Research Unit, National
Animal Disease Center, ARS, USDA, Ames, IA provided a presentation on scrapie
and CWD in inoculated deer. Interspecies transmission studies afford the
opportunity to better understand the potential host range and origins of prion
diseases. We inoculated white-tailed deer intracranially (IC) and by a natural
route of exposure (concurrent oral and intranasal inoculation) with a US scrapie
isolate. All deer inoculated by the intracranial route had evidence of PrPSc
accumulation and those necropsied after 20 months post-inoculation (PI) (3/5)
had clinical signs, spongiform encephalopathy, and widespread distribution of
PrPSc in neural and lymphoid tissues. A single deer that was necropsied at 15.6
months PI did not have clinical signs, but had widespread distribution of PrPSc.
This highlights the facts that 1) prior to the onset of clinical signs PrPSc is
widely distributed in the CNS and lymphoid tissues and 2) currently used
diagnostic methods are sufficient to detect PrPSc prior to the onset of clinical
signs. The results of this study suggest that there are many similarities in the
manifestation of CWD and scrapie in white-tailed deer after IC inoculation
including early and widespread presence of PrPSc in lymphoid tissues, clinical
signs of depression and weight loss progressing to wasting, and an incubation
time of 21-23 months. Moreover, western blots (WB) done on brain material from
the obex region have a molecular profile consistent with CWD and distinct from
tissues of the cerebrum or the scrapie inoculum. However, results of microscopic
and IHC examination indicate that there are differences between the lesions
expected in CWD and those that occur in deer with scrapie: amyloid plaques were
not noted in any sections of brain examined from these deer and the pattern of
immunoreactivity by IHC was diffuse rather than plaque-like. After a natural
route of exposure, 100% of white-tailed deer were susceptible to scrapie. Deer
developed clinical signs of wasting and mental depression and were necropsied
from 28 to 33 months PI. Tissues from these deer were positive for scrapie by
IHC and WB. Tissues with PrPSc immunoreactivity included brain, tonsil,
retropharyngeal and mesenteric lymph nodes, hemal node, Peyer’s patches, and
spleen. While two WB patterns have been detected in brain regions of deer
inoculated by the natural route, unlike the IC inoculated deer, the pattern
similar to the scrapie inoculum predominates.
Committee Business:
The Committee discussed and approved three resolutions regarding CWD. They
can be found in the report of the Reswolutions Committee. Essentially the
resolutions urged USDA-APHIS-VS to:
Continue to provide funding for CWD testing of captive cervids
Finalize and publish the national CWD rule for Herd Certification and
Interstate Movement
Evaluate live animal test, including rectal mucosal biopsy, for CWD in
cervids
5. A positive result from a chimpanzee challenged severely 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.
Wednesday, February 16, 2011
IN CONFIDENCE SCRAPIE TRANSMISSION TO CHIMPANZEES IN CONFIDENCE
reference...
RB3.20 TRANSMISSION TO CHIMPANZEES
1. Kuru and CJD have been successfully transmitted to chimpanzees but
scrapie and TME have not.
2. We cannot say that scrapie will not transmit to chimpanzees. There are
several scrapie strains and I am not aware that all have been tried (that would
have to be from mouse passaged material). Nor has a wide enough range of field
isolates subsequently strain typed in mice been inoculated by the appropriate
routes (i/c, ilp and i/v) :
3. I believe the proposed experiment to determine transmissibility, if
conducted, would only show the susceptibility or resistance of the chimpanzee to
infection/disease by the routes used and the result could not be interpreted for
the predictability of the susceptibility for man. Proposals for prolonged oral
exposure of chimpanzees to milk from cattle were suggested a long while ago and
rejected.
4. In view of Dr Gibbs' probable use of chimpazees Mr Wells' comments
(enclosed) are pertinent. I have yet to receive a direct communication from Dr
Schellekers but before any collaboration or provision of material we should
identify the Gibbs' proposals and objectives.
5. A positive result from a chimpanzee challenged severely 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.
6. A negative result would take a lifetime to determine but that would be a
shorter period than might be available for human exposure and it would still not
answer the question regarding mans' susceptibility. In the meantime no doubt the
negativity would be used defensively. It would however be counterproductive if
the experiment finally became positive. We may learn more about public reactions
following next Monday' s meeting.
R. Bradley 23 September 1990 CVO (+Mr Wells' comments) Dr T W A Little Dr B
J Shreeve 90/9.23/1.1.
see more here ;
Rabbits are not resistant to prion infection
Francesca Chianinia,1, Natalia Fernández-Borgesb,c,1, Enric Vidald, Louise
Gibbarda, Belén Pintadoe, Jorge de Castroc, Suzette A. Priolaf, Scott Hamiltona,
Samantha L. Eatona, Jeanie Finlaysona, Yvonne Panga, Philip Steelea, Hugh W.
Reida, Mark P. Dagleisha, and Joaquín Castillab,c,g,2
snip...
Discussion
Slightly more than 25 y ago, cattle were considered free of prion diseases.
No one would have predicted the BSE epidemic with the considerable human and
animal health repercussions, and the political and economic impacts that it had
in Europe during the 1990s. At that time, the scientific knowledge of prions was
too limited to determine its role in the development of spontaneous cases of BSE
and their subsequent impact on human health. By 2011, however, several new prion
strains, naturally occurring (19, 20) or artificially generated (10), have been
described, indicating that their number has increased and that a species should
be considered resistant to disease only after careful consideration. The degree
of resistance and susceptibility to prion disease(s) differs within species.
Animals can be both extremely susceptible to the majority of prion diseases or
strains yet remain resistant to others on first passage (21). Therefore, it
would be unwise to assume that a species generally resistant to TSEs would
represent a minor risk to human health, as new TSEs and strains are continually
being detected.
It is notoriously difficult to predict how a new TSE or strain will behave
in different species, so great caution must be exercised when determining the
transmissibility of prions between species. To evaluate the potential risk of
transmission, every tool in the prion toolkit is essential, including artificial
methods, such as the use of transgenic animals, or secondary in vivo
transmission, which can exaggerate the possibility of infection (2, 22).
Even these extreme measures, which probably do not reflect the normal
mechanisms of infection, have to be considered to avoid future epidemics similar
to that observed with the new variant Creutzfeldt-Jakob disease (vCJD). For this
reason, we selected PMCA with its associated advantages, including the ability
to overcome the transmission barrier (8), as the preferred tool to evaluate the
absolute susceptibility of rabbits to TSEs.
Using only normal rabbit brain homogenate as a substrate for PMCA, PrPC was
efficiently converted to rabbit PrPres when seeded with strains originating from
four different species (Table 1), and at least three biochemically
distinguishable rabbit PrPres strains were obtained (Fig. 1). This suggests that
rabbit PrPC is more readily misfolded than originally thought. However, a prion
disease is more than a simple misfolding process, and other factors are probably
required for successful disease progression in vivo.
To address this point, we inoculated three groups of rabbits, two groups
with ME7 based inocula (murine and leporine) and a further group with the de
novo rabbit PMCA derived PrPres. Selection of these particular strains was
carried out on the basis that ME7 was stable and well characterized and the de
novo strain was an unknown entity. The number of strains tested and rabbits
challenged were limited because of the necessity of housing these animals in
containment level 3 facilities for protracted periods of time that maximized the
possibility of transmission and development of disease.
Although rabbits were inoculated with prions derived from the same species,
a 25-mo period was necessary to observe the standard prion disease. The three
animals that died without clinical signs of TSE were all negative by IHC and WB,
although the first of these deaths was in a rabbit challenged with ME7 RaPrPSc,
which had PrPSc levels in the brain detectable only by PMCA. This result
indicates that even though the animal died of a non– TSE-related disease, it
might have been at an early preclinical stage of prion disease. However, we
cannot rule out the possibility that the limited PrPSc level in the brain sample
was due to residual inoculum, as shown previously in PrP knock-out mice (23). To
date, the rabbits inoculated with mouse ME7 remain healthy after more than 43
mo, which is in agreement with the experiments performed approximately 35 y ago
by Barlow and Rennie (17).
In summary, after 3 y postchallenge with three different rabbitderived
inocula, we have obtained one positive clinical case, one possible preclinical
case, two intercurrent deaths, and six animals that have remained healthy.
Although the incubation periods do not directly correlate with the degree of
susceptibility, these data might indicate that rabbits are poorly susceptible to
prion infection. Although the rabbits used in this study were not inbred, they
all had identical full-length PrP sequences and, to date, no difference has been
detected in the ORF PrP sequence in any other published rabbit PrP sequence
placed in GenBank. To further investigate this, two types of second passage
experiment were performed; three raPrPTg mice and 10 rabbits were all
intracerebrally inoculated using brain homogenate from the clinically affected
rabbit. In contrast to 100% of the de novo RaPrPSc-inoculated transgenic mice
having succumbed to a standard clinical prion disease and thereby demonstrating
a high rate of transmissibility in vivo, two of 10 rabbits developed a TSE (477
and 540 dpi, respectively) to date. A plausible explanation for the evident
differences between these two transmission studies would be the high level of
rabbit PrPC expression (4- to 6-fold) in the murine model. In addition, it is
well known that even if overexpression does not increase susceptibility, it can
significantly reduce the incubation time of disease (2). However, the two
positive TSE cases in the second rabbit passage, even though 8 rabbits remained
clinically normal at 560 dpi, have led us to conclude that rabbits can no longer
be considered a prionresistant species. The long incubation times, even after a
second passage, might be due to the presence of some unknown, and probably rare,
susceptibility factor in rabbits, which may also be present, for example, in
equids and canids.
To critically evaluate this risk, several experiments are currently
underway to characterize this new prion disease in rabbits and other species to
examine its ability to cross the species barrier. In addition, supplementary
experiments have been initiated in rabbits and also in transgenic mice that
overexpress rabbit PrPC, to evaluate their susceptibilities to other important
prion diseases including CWD and BSE. There are several factors that any
potential new TSE epidemic would require: (i) the new prion should be
efficiently transmitted through the homologous species; (ii) animals should be
edible by humans and should be slaughtered at an age at which the disease has
developed, thereby increasing the chance that prions have replicated (especially
for those prions that require long incubation times); and (iii) the meat and
bone meal should be recycled and fed to new members of the same species. In the
light of these data and taking into account the previous three factors, it is
unlikely there will be an outbreak of “mad rabbit disease,” and consumers of
rabbit meat face much less of a risk than consumers of cattle or sheep products.
> The long incubation times, even after a second passage, might be due
to the presence of some unknown, and probably rare, susceptibility factor in
rabbits, which may also be present, for example, in equids and canids.
> equids and canids
TSE in dogs have not been documented simply because OF THE ONLY STUDY,
those brain tissue samples were screwed up too. see my investigation of this
here, and to follow, later follow up, a letter from defra, AND SEE SUSPICIOUS
BRAIN TISSUE SAF's. ...TSS
TSE & HOUNDS
GAH WELLS (very important statement here...TSS)
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...
76 pages on hound study;
The spongiform changes were not pathognomonic (ie. conclusive proof) for
prion disease, as they were atypical, being largely present in white matter
rather than grey matter in the brain and spinal cord. However, Tony Scott, then
head of electron microscopy work on TSEs, had no doubt that these SAFs were
genuine and that these hounds therefore must have had a scrapie-like disease. I
reviewed all the sections myself (original notes appended) and although the
pathology was not typical, I could not exclude the possibility that this was a
scrapie-like disorder, as white matter vacuolation is seen in TSEs and Wallerian
degeneration was also present in the white matter of the hounds, another feature
of scrapie.
38.I reviewed the literature on hound neuropathology, and discovered that
micrographs and descriptive neuropathology from papers on 'hound ataxia'
mirrored those in material from Robert Higgins' hound survey. Dr Tony Palmer
(Cambridge) had done much of this work, and I obtained original sections from
hound ataxia cases from him. This enabled me provisionally to conclude that
Robert Higgins had in all probability detected hound ataxia, but also that hound
ataxia itself was possibly a TSE. Gerald Wells confirmed in 'blind' examination
of single restricted microscopic fields that there was no distinction between
the white matter vacuolation present in BSE and scrapie cases, and that
occurring in hound ataxia and the hound survey cases.
39.Hound ataxia had reportedly been occurring since the 1930's, and a known
risk factor for its development was the feeding to hounds of downer cows, and
particularly bovine offal. Circumstantial evidence suggests that bovine offal
may also be causal in FSE, and TME in mink. Despite the inconclusive nature of
the neuropathology, it was clearly evident that this putative canine spongiform
encephalopathy merited further investigation.
40.The inconclusive results in hounds were never confirmed, nor was the
link with hound ataxia pursued. I telephoned Robert Higgins six years after he
first sent the slides to CVL. I was informed that despite his submitting a
yearly report to the CVO including the suggestion that the hound work be
continued, no further work had been done since 1991. This was surprising, to say
the very least.
41.The hound work could have provided valuable evidence that a scrapie-like
agent may have been present in cattle offal long before the BSE epidemic was
recognised. The MAFF hound survey remains unpublished.
Histopathological support to various other published MAFF experiments
42.These included neuropathological examination of material from
experiments studying the attempted transmission of BSE to chickens and pigs (CVL
1991) and to mice (RVC 1994).
It was thought likely that at least some, and probably all, of the cases in
zoo animals were caused by the BSE agent. Strong support for this hypothesis
came from the findings of Bruce and others (1994) ( Bruce, M.E., Chree, A.,
McConnell, I., Foster, J., Pearson, G. & Fraser, H. (1994) Transmission of
bovine spongiform encephalopathy and scrapie to mice: strain variation and
species barrier. Philosophical Transactions of the Royal Society B 343, 405-411:
J/PTRSL/343/405 ), who demonstrated that the pattern of variation in incubation
period and lesion profile in six strains of mice inoculated with brain
homogenates from an affected kudu and the nyala, was similar to that seen when
this panel of mouse strains was inoculated with brain from cattle with BSE. The
affected zoo bovids were all from herds that were exposed to feeds that were
likely to have contained contaminated ruminant-derived protein and the zoo
felids had been exposed, if only occasionally in some cases, to tissues from
cattle unfit for human consumption.
snip...
2005
DEFRA Department for Environment, Food & Rural Affairs
Area 307, London, SW1P 4PQ Telephone: 0207 904 6000 Direct line: 0207 904
6287 E-mail: h.mcdonagh.defra.gsi.gov.uk
GTN: FAX:
Mr T S Singeltary P.O. Box 42 Bacliff Texas USA 77518
21 November 2001
Dear Mr Singeltary
TSE IN HOUNDS
Thank you for e-mail regarding the hounds survey. I am sorry for the long
delay in responding.
As you note, the hound survey remains unpublished. However the Spongiform
Encephalopathy Advisory Committee (SEAC), the UK Government's independent
Advisory Committee on all aspects related to BSE-like disease, gave the hound
study detailed consideration at their meeting in January 1994. As a summary of
this meeting published in the BSE inquiry noted, the Committee were clearly
concerned about the work that had been carried out, concluding that there had
clearly been problems with it, particularly the control on the histology, and
that it was more or less inconclusive. However was agreed that there should be a
re-evaluation of the pathological material in the study.
Later, at their meeting in June 95, The Committee re-evaluated the hound
study to see if any useful results could be gained from it. The Chairman
concluded that there were varying opinions within the Committee on further work.
It did not suggest any further transmission studies and thought that the lack of
clinical data was a major weakness.
Overall, it is clear that SEAC had major concerns about the survey as
conducted. As a result it is likely that the authors felt that it would not
stand up to r~eer review and hence it was never published. As noted above, and
in the detailed minutes of the SEAC meeting in June 95, SEAC considered whether
additional work should be performed to examine dogs for evidence of TSE
infection. Although the Committee had mixed views about the merits of conducting
further work, the Chairman noted that when the Southwood Committee made their
recommendation to complete an assessment of possible spongiform disease in dogs,
no TSEs had been identified in other species and hence dogs were perceived as a
high risk population and worthy of study. However subsequent to the original
recommendation, made in 1990, a number of other species had been identified with
TSE ( e.g. cats) so a study in hounds was less
critical. For more details see- http://www.bseinquiry,
gov.uk/files/yb/1995/06/21005001 .pdf
As this study remains unpublished, my understanding is that the ownership
of the data essentially remains with the original researchers. Thus
unfortunately, I am unable to help with your request to supply information on
the hound survey directly. My only suggestion is that you contact one of the
researchers originally involved in the project, such as Gerald Wells. He can be
contacted at the following address.
Dr Gerald Wells, Veterinary Laboratories Agency, New Haw, Addlestone,
Surrey, KT 15 3NB, UK
You may also wish to be aware that since November 1994 all suspected cases
of spongiform encephalopathy in animals and poultry were made notifiable. Hence
since that date there has been a requirement for vets to report any suspect SE
in dogs for further investigation. To date there has never been positive
identification of a TSE in a dog.
I hope this is helpful
Yours sincerely 4
HUGH MCDONAGH BSE CORRESPONDENCE SECTION
======================================
FAST FORWARD 2012
From: Terry S. Singeltary Sr. Sent: Wednesday, May 30, 2012 12:23 PM To:
Terry S. Singeltary Sr. Subject: CANINE SPONGIFORM ENCEPHALOPATHY: A NEW FORM OF
ANIMAL PRION DISEASE
OR-09: Canine spongiform encephalopathy—A new form of animal prion disease
Monique David, Mourad Tayebi UT Health; Houston, TX USA
It was also hypothesized that BSE might have originated from an
unrecognized sporadic or genetic case of bovine prion disease incorporated into
cattle feed or even cattle feed contaminated with prion-infected human remains.1
However, strong support for a genetic origin of BSE has recently been
demonstrated in an H-type BSE case exhibiting the novel mutation E211K.2
Furthermore, a specific prion protein strain causing BSE in cattle is believed
to be the etiological agent responsible for the novel human prion disease,
variant Creutzfeldt-Jakob disease (vCJD).3 Cases of vCJD have been identified in
a number countries, including France, Italy, Ireland, the Netherlands, Canada,
Japan, US and the UK with the largest number of cases. Naturally occurring
feline spongiform encephalopathy of domestic cats4 and spongiform
encephalopathies of a number of zoo animals so-called exotic ungulate
encephalopathies5,6 are also recognized as animal prion diseases, and are
thought to have resulted from the same BSE-contaminated food given to cattle and
humans, although and at least in some of these cases, a sporadic and/or genetic
etiology cannot be ruled out. The canine species seems to display resistance to
prion disease and no single case has so far been reported.7,8 Here, we describe
a case of a 9 week old male Rottweiler puppy presenting neurological deficits;
and histological examination revealed spongiform vacuolation characteristic of
those associated with prion diseases.9 Initial biochemical studies using
anti-PrP antibodies revealed the presence of partially proteinase K-resistant
fragment by western blotting. Furthermore, immunohistochemistry revealed
spongiform degeneration consistent with those found in prion disease and
displayed staining for PrPSc in the cortex.
Of major importance, PrPSc isolated from the Rottweiler was able to cross
the species barrier transmitted to hamster in vitro with PMCA and in vivo (one
hamster out of 5). Futhermore, second in vivo passage to hamsters, led to 100%
attack rate (n = 4) and animals displayed untypical lesional profile and shorter
incubation period.
In this study, we show that the canine species might be sensitive to prion
disease and that PrPSc isolated from a dog can be transmitted to dogs and
hamsters in vitro using PMCA and in vivo to hamsters.
If our preliminary results are confirmed, the proposal will have a major
impact on animal and public health and would certainly lead to implementing new
control measures for ‘canine spongiform encephalopathy’ (CSE).
References 1. Colchester AC, Colchester NT. The origin of bovine spongiform
encephalopathy: the human prion disease hypothesis. Lancet 2005; 366:856-61;
PMID:16139661; http://
dx.doi.org/10.1016/S0140-6736(05)67218-2.
2. Richt JA, Hall SM. BSE case associated with prion protein gene mutation.
PLoS Pathog 2008; 4:e1000156; PMID:18787697; http://dx.doi.org/10.1371/journal.
ppat.1000156.
3. Collinge J. Human prion diseases and bovine spongiform encephalopathy
(BSE). Hum Mol Genet 1997; 6:1699-705; PMID:9300662; http://dx.doi.org/10.1093/
hmg/6.10.1699.
4. Wyatt JM, Pearson GR, Smerdon TN, Gruffydd-Jones TJ, Wells GA, Wilesmith
JW. Naturally occurring scrapie-like spongiform encephalopathy in five domestic
cats. Vet Rec 1991; 129:233-6; PMID:1957458; http://dx.doi.org/10.1136/vr.129.11.233.
5. Jeffrey M, Wells GA. Spongiform encephalopathy in a nyala (Tragelaphus
angasi). Vet Pathol 1988; 25:398-9; PMID:3232315; http://dx.doi.org/10.1177/030098588802500514.
6. Kirkwood JK, Wells GA, Wilesmith JW, Cunningham AA, Jackson SI.
Spongiform encephalopathy in an arabian oryx (Oryx leucoryx) and a greater kudu
(Tragelaphus strepsiceros). Vet Rec 1990; 127:418-20; PMID:2264242.
7. Bartz JC, McKenzie DI, Bessen RA, Marsh RF, Aiken JM. Transmissible mink
encephalopathy species barrier effect between ferret and mink: PrP gene and
protein analysis. J Gen Virol 1994; 75:2947-53; PMID:7964604; http://dx.doi.org/10.1099/0022-1317-
75-11-2947.
8. Lysek DA, Schorn C, Nivon LG, Esteve-Moya V, Christen B, Calzolai L, et
al. Prion protein NMR structures of cats, dogs, pigs, and sheep. Proc Natl Acad
Sci U S A 2005; 102:640-5; PMID:15647367; http://dx.doi.org/10.1073/pnas.0408937102.
9. Budka H. Neuropathology of prion diseases. Br Med Bull 2003; 66:121-30;
PMID:14522854; http://dx.doi.org/10.1093/bmb/66.1.121.
Monday, March 26, 2012
CANINE SPONGIFORM ENCEPHALOPATHY: A NEW FORM OF ANIMAL PRION DISEASE
http://caninespongiformencephalopathy.blogspot.com/2012/03/canine-spongiform-encephalopathy-new.html
IN CONFIDENCE
SUSPECT BSE IN A HORSE
CYO BSE 1 9
IN CONFIDENCE
SUSPECT BSE IN A HORSE
The Parliamentary Secretary (Mr Maclean) will wish to be aware that, in
making his differential diagnosis, a veterinary surgeon in the Reading area has
included the possibility of BSE in a horse under his care. Although it is
unlikely to be BSE, because of the symptoms exhibited the veterinarian believes
that he cannot exclude the possibility. The case was brought to the notice of
one of the veterinary staff at the CVL by the owner's veterinary surgeon and
liaison is being maintained.
The horse in question is a five-year old eventing gelding which was
purchased by the present owner about four months ago. Approximately two months
after purchase the animal became a little apprehensive, developed mild nervous
symptoms and became over-sensitive to noise. The nervous symptoms have increased
and the horse is now practically impossible to ride. Investigations by the
owner's private veterinary surgeon are continuing but it is likely that the
animal will have to be destroyed.
If the horse should die or be destroyed, a full post-mortem examination
will be required for insurance purposes and will probably be carried out at a
non-Ministry laboratory. However, Mr Bradley of the Pathology Department, CVL,
has informed the private veterinary surgeon that he is willing to provide a
second opinion on the brain histology if requested.
I will keep the Parliamentary Secretary informed of any further
developments in the case.
I CRAWFORD
14 May 1990
Mr M P H Hill, PS/Parliamentary secretary (Mr Maclean) - by FAX
cc:
Private Offices
Mr K C Meldrum
Mrs E A J Attridge D J Evans Mr K C Taylor Mr R Lawson Mr R Bradley. CVL
(hand written notes i cannot read all (cut short) as follows...tss)
The Parliamentary Secretary (Mr Maclean was grateful for this. He said that
we must keep very close to ...on it, and when the horse dies, or is put down we
must be told immediately. He also feels it is very important that our veterinary
staff be involved in the brain examination. .........(cannot read the rest
.............TSS)
90/05.14/10.1
Mr A Huws Principal WOAD2A CP2
SUSPECT BSE IN A HORSE
You will wish to be aware that on Thursday afternoon 25 June the T/DVO
Powys received a phone call from a veterinary Surgeon reporting his suspicion
that a horse had ___contracted BSE after having been fed cattle cake___.
The clinical symptoms described were similar to those shown by cattle there
___being a similar case some months ago on the same premises___.
The owner' s name and address is:
Irene Thomas J Thomas & Company Riding Stables Penybryn Llangorse
Brecon
The horse is a 12 year old gelding used for pony trekking.
By yesterday evening the horse was in a comatose state and on humane
grounds was destroyed by the veterinary Surgeon. At his request a full post
mortem and laboratory investigation will be carried out at the Carmarthen
Veterinary Investigation Centre this morning to ascertain the exact cause; I
have been told this will take at least two weeks. Charges to the veterinary
Surgeon have been waived in this instance.
I will inform you immediately I receive a diagnosis.
26 June 1990
D SUMMERS DRVO
cc
Mr D R Williams, RVO
Mr A R Hunter, SVIO
90/06.26/10.1
Mr A Huws Principal WOAD2A CP2
SUSPECT BSE IN A HORSE
You will wish to be aware that on Thursday afternoon 25 June the T/DVO
Powys received a phone call from a veterinary Surgeon reporting his suspicion
that a horse had contracted BSE after having been fed cattle cake. The clinical
symptoms described were similar to those shown by cattle there being a similar
case some months ago on the same premises.
The owner' s name and address is:
Irene Thomas J Thomas & Company Riding Stables Penybryn Llangorse
Brecon
The horse is a 12 year old gelding used for pony trekking.
By yesterday evening the horse was in a comatose state and on humane
grounds was destroyed by the veterinary Surgeon. At his request a full post
mortem and laboratory investigation will be carried out at the Carmarthen
Veterinary Investigation Centre this morning to ascertain the exact cause; I
have been told this will take at least two weeks. Charges to the veterinary
Surgeon have been waived in this instance.
I will inform you immediately I receive a diagnosis.
26 June 1990
D SUMMERS DRVO
cc
Mr D R Williams, RVO
Mr A R Hunter, SVIO
90/06.26/10.1
see full text and more here ;
>>> The most widely accepted hypothesis at this time is that CWD
may have originated from an interspecies transmission of scrapie. It is worth
noting that experimental transmission of scrapie into elk via IC inoculation is
clinically and neuropathologically indistinguishable from CWD with currently
available experimental methods.44 <<<
2011 Annual Report
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES Location: Virus and Prion Research
Unit
2011 Annual Report
In Objective 1, Assess cross-species transmissibility of transmissible
spongiform encephalopathies (TSEs) in livestock and wildlife, numerous
experiments assessing the susceptibility of various TSEs in different host
species were conducted. Most notable is deer inoculated with scrapie, which
exhibits similarities to chronic wasting disease (CWD) in deer suggestive of
sheep scrapie as an origin of CWD.
snip...
4.Accomplishments 1. Deer inoculated with domestic isolates of sheep
scrapie. Scrapie-affected deer exhibit 2 different patterns of disease
associated prion protein. In some regions of the brain the pattern is much like
that observed for scrapie, while in others it is more like chronic wasting
disease (CWD), the transmissible spongiform encephalopathy typically associated
with deer. This work conducted by ARS scientists at the National Animal Disease
Center, Ames, IA suggests that an interspecies transmission of sheep scrapie to
deer may have been the origin of CWD. This is important for husbandry practices
with both captive deer, elk and sheep for farmers and ranchers attempting to
keep their herds and flocks free of CWD and scrapie.
White-tailed Deer are Susceptible to Scrapie by Natural Route of Infection
Jodi D. Smith, Justin J. Greenlee, and Robert A. Kunkle; Virus and Prion
Research Unit, National Animal Disease Center, USDA-ARS
Interspecies transmission studies afford the opportunity to better
understand the potential host range and origins of prion diseases. Previous
experiments demonstrated that white-tailed deer are susceptible to sheep-derived
scrapie by intracranial inoculation. The purpose of this study was to determine
susceptibility of white-tailed deer to scrapie after a natural route of
exposure. Deer (n=5) were inoculated by concurrent oral (30 ml) and intranasal
(1 ml) instillation of a 10% (wt/vol) brain homogenate derived from a sheep
clinically affected with scrapie. Non-inoculated deer were maintained as
negative controls. All deer were observed daily for clinical signs. Deer were
euthanized and necropsied when neurologic disease was evident, and tissues were
examined for abnormal prion protein (PrPSc) by immunohistochemistry (IHC) and
western blot (WB). One animal was euthanized 15 months post-inoculation (MPI)
due to an injury. At that time, examination of obex and lymphoid tissues by IHC
was positive, but WB of obex and colliculus were negative. Remaining deer
developed clinical signs of wasting and mental depression and were necropsied
from 28 to 33 MPI. Tissues from these deer were positive for scrapie by IHC and
WB. Tissues with PrPSc immunoreactivity included brain, tonsil, retropharyngeal
and mesenteric lymph nodes, hemal node, Peyer’s patches, and spleen. This work
demonstrates for the first time that white-tailed deer are susceptible to sheep
scrapie by potential natural routes of inoculation. In-depth analysis of tissues
will be done to determine similarities between scrapie in deer after
intracranial and oral/intranasal inoculation and chronic wasting disease
resulting from similar routes of inoculation.
see full text ;
Chronic Wasting Disease Q&A from St. Joseph MO MDC meeting claimed ;
>>>animal to animal, prions in urine, deer social animals,
environmental contamination, exposed in the environment, why we did the feed and
mineral ban. there is no vector for disease other than the social contact or
prion in the soil...?
NOT EXACTLY TRUE, oral consumption from animal protein in feed is highly
efficient mode of transmission for chronic wasting disease cwd, and the infamous
mad cow feed ban was, and is still a seriously flawed system, please see ;
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...
PLEASE SEE FULL TEXT SUBMISSION ;
Date: Tue, 24 Apr 2001 09:45:15 –0700
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy
To: BSE-L@uni-karlsruhe.de References: 1 , 2
######### Bovine Spongiform Encephalopathy #########
Greetings again List Members,
''MORE'' violations and warning letters over FDA MAD COW feed ban
regulations that have not been complied with since the Aug. 4, 1997 'partial'
feed ban was implemented...
they implemented something, then forgot to enforce it $$$$$
another fine example letter. this one will floor you. 'Jimmy crack corn,
and they don't care' no big deal, just flush those mixers with corn, then feed
the corn to the deer. NOooooo problem.
these people must be brain dead???
DEPARTMENT OF HEALTH & HUMAN SERVICES PUBLIC HEALTH SERVICE FOOD AND
DRUG ADMINISTRATION
April 9, 2001 WARNING LETTER
01-PHI-12 CERTIFIED MAIL RETURN RECEIPT REQUESTED
Brian J. Raymond, Owner Sandy Lake Mills 26 Mill Street P.O. Box 117 Sandy
Lake, PA 16145 PHILADELPHIA DISTRICT
Tel: 215-597-4390
Dear Mr. Raymond:
Food and Drug Administration Investigator Gregory E. Beichner conducted an
inspection of your animal feed manufacturing operation, located in Sandy Lake,
Pennsylvania, on March 23, 2001, and determined that your firm manufactures
animal feeds including feeds containing prohibited materials. The inspection
found significant deviations from the requirements set forth in Title 21, code
of Federal Regulations, part 589.2000 - Animal Proteins Prohibited in Ruminant
Feed. The regulation is intended to prevent the establishment and amplification
of Bovine Spongiform Encephalopathy (BSE) . Such deviations cause products being
manufactured at this facility to be misbranded within the meaning of Section
403(f), of the Federal Food, Drug, and Cosmetic Act (the Act).
Our investigation found failure to label your swine feed with the required
cautionary statement "Do Not Feed to cattle or other Ruminants" The FDA suggests
that the statement be distinguished by different type-size or color or other
means of highlighting the statement so that it is easily noticed by a purchaser.
In addition, we note that you are using approximately 140 pounds of cracked
corn to flush your mixer used in the manufacture of animal feeds containing
prohibited material. This flushed material is fed to wild game including deer, a
ruminant animal. Feed material which may potentially contain prohibited material
should not be fed to ruminant animals which may become part of the food chain.
The above is not intended to be an all-inclusive list of deviations from
the regulations. As a manufacturer of materials intended for animal feed use,
you are responsible for assuring that your overall operation and the products
you manufacture and distribute are in compliance with the law. We have enclosed
a copy of FDA's Small Entity Compliance Guide to assist you with complying with
the regulation... blah, blah, blah...
-------- Original Message --------
Subject: MAD DEER FEED BAN WARNING LETTER RECALL 6 TONS DISTRIBUTED
USA
Date: Wed, 20 Oct 2004 14:53:56 –0500
From: "Terry S. Singeltary Sr." flounder@WT.NET
Reply-To: Bovine Spongiform Encephalopathy BSE-L@UNI-KARLSRUHE.DE
To: BSE-L@UNI-KARLSRUHE.DE
##################### Bovine Spongiform Encephalopathy
#####################
PRODUCT
Product is __custom made deer feed__ packaged in 100 lb. poly bags. The
product has no labeling. Recall # V-003-5.
CODE
The product has no lot code. All custom made feed purchased between June
24, 2004 and September 8, 2004.
RECALLING FIRM/MANUFACTURER
Farmers Elevator Co, Houston, OH, by telephone and letter dated September
27, 2004. Firm initiated recall is ongoing.
REASON
Feed may contain protein derived from mammalian tissues which is prohibited
in ruminant feed.
VOLUME OF PRODUCT IN COMMERCE
Approximately 6 tons.
DISTRIBUTION OH.
END OF ENFORCEMENT REPORT FOR October 20, 2004
################# BSE-L-subscribe-request@uni-karlsruhe.de
#################
DOCKET-- 03D-0186 -- FDA Issues Draft Guidance on Use of Material From Deer
and Elk in Animal Feed; Availability
Date: Fri, 16 May 2003 11:47:37 –0500
EMC 1 Terry S. Singeltary Sr. Vol #: 1
Thursday, June 6, 2013
BSE TSE PRION USDA FDA MAD COW FEED COMPLIANCE REPORT and NAI, OAI, and VAI
ratings as at June 5, 2013
Friday, July 19, 2013
PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED Revised
as of April 1, 2013 50# Regular Chicken Feed was found to contain mammalian
protein label does not contain the warning statement
Tuesday, June 11, 2013
Weld County Bi-Products dba Fort Morgan Pet Foods 6/1/12 significant
deviations from requirements in FDA regulations that are intended to reduce the
risk of bovine spongiform encephalopathy (BSE) within the United States
Wednesday, September 25, 2013
Inspections, Compliance, Enforcement, and Criminal Investigations BSE TSE
PRION 2013
Chronic Wasting Disease Q&A from St. Joseph MO MDC meeting claimed ;
>>>if you have only one or two not much of a problem, but once
the count numbers go up, so does the load of cwd in the environment. ...probably
diluted out, it’s all about how many animals infected, before environmental
contamination takes over?
that’s not completely correct either. ...FEED, captive game farms, and
transfer of tainted soil via humans and vehicles, plants, shoes, clothing, etc.,
don’t believe me, see what the U.K. MAFF/DEFRA are saying ;
Friday, December 14, 2012
DEFRA U.K. What is the risk of Chronic Wasting Disease CWD being introduced
into Great Britain? A Qualitative Risk Assessment October 2012
snip...
In the USA, under the Food and Drug Administration’s BSE Feed Regulation
(21 CFR 589.2000) most material (exceptions include milk, tallow, and gelatin)
from deer and elk is prohibited for use in feed for ruminant animals. With
regards to feed for non-ruminant animals, under FDA law, CWD positive deer may
not be used for any animal feed or feed ingredients.
*** For elk and deer considered at high risk for CWD, the FDA recommends
that these animals do not enter the animal feed system.
*** However, this recommendation is guidance and not a requirement by law.
Animals considered at high risk for CWD include:
1) animals from areas declared to be endemic for CWD and/or to be CWD
eradication zones and
2) deer and elk that at some time during the 60-month period prior to
slaughter were in a captive herd that contained a CWD-positive animal.
Therefore, in the USA, materials from cervids other than CWD positive
animals may be used in animal feed and feed ingredients for non-ruminants.
The amount of animal PAP that is of deer and/or elk origin imported from
the USA to GB can not be determined, however, as it is not specified in TRACES.
It may constitute a small percentage of the 8412 kilos of non-fish origin
processed animal proteins that were imported from US into GB in 2011.
Overall, therefore, it is considered there is a __greater than negligible
risk___ that (nonruminant) animal feed and pet food containing deer and/or elk
protein is imported into GB.
There is uncertainty associated with this estimate given the lack of data
on the amount of deer and/or elk protein possibly being imported in these
products.
snip...
36% in 2007 (Almberg et al., 2011). In such areas, population declines of
deer of up to 30 to 50% have been observed (Almberg et al., 2011). In areas of
Colorado, the prevalence can be as high as 30% (EFSA, 2011).
The clinical signs of CWD in affected adults are weight loss and
behavioural changes that can span weeks or months (Williams, 2005). In addition,
signs might include excessive salivation, behavioural alterations including a
fixed stare and changes in interaction with other animals in the herd, and an
altered stance (Williams, 2005). These signs are indistinguishable from cervids
experimentally infected with bovine spongiform encephalopathy (BSE).
Given this, if CWD was to be introduced into countries with BSE such as GB,
for example, infected deer populations would need to be tested to differentiate
if they were infected with CWD or BSE to minimise the risk of BSE entering the
human food-chain via affected venison.
snip...
The rate of transmission of CWD has been reported to be as high as 30% and
can approach 100% among captive animals in endemic areas (Safar et al., 2008).
snip...
In summary, in endemic areas, there is a medium probability that the soil
and surrounding environment is contaminated with CWD prions and in a
bioavailable form. In rural areas where CWD has not been reported and deer are
present, there is a greater than negligible risk the soil is contaminated with
CWD prion.
snip...
In summary, given the volume of tourists, hunters and servicemen moving
between GB and North America, the probability of at least one person travelling
to/from a CWD affected area and, in doing so, contaminating their clothing,
footwear and/or equipment prior to arriving in GB is greater than negligible.
For deer hunters, specifically, the risk is likely to be greater given the
increased contact with deer and their environment. However, there is significant
uncertainty associated with these estimates.
snip...
Therefore, it is considered that farmed and park deer may have a higher
probability of exposure to CWD transferred to the environment than wild deer
given the restricted habitat range and higher frequency of contact with tourists
and returning GB residents.
snip...
see full text report here ;
see much more here ;
Friday, December 14, 2012
DEFRA U.K. What is the risk of Chronic Wasting Disease CWD being introduced
into Great Britain? A Qualitative Risk Assessment October 2012
Chronic Wasting Disease Q&A from St. Joseph MO MDC meeting claimed ;
>>>> NO THREAT TO CATTLE HERDS ?
CWD TO CATTLE OR BSE TO CERVIDS, potential risk factors ??? LET’S see what
the science says to date ;
UPDATED DATA ON 2ND CWD STRAIN
Wednesday, September 08, 2010
CWD PRION CONGRESS SEPTEMBER 8-11 2010
UPDATED CORRESPONDENCE FROM AUTHORS OF THIS STUDY I.E. COLBY, PRUSINER ET
AL, ABOUT MY CONCERNS OF THE DISCREPANCY BETWEEN THEIR FIGURES AND MY FIGURES OF
THE STUDIES ON CWD TRANSMISSION TO CATTLE ;
CWD to cattle figures CORRECTION
Greetings,
I believe the statement and quote below is incorrect ;
"CWD has been transmitted to cattle after intracerebral inoculation,
although the infection rate was low (4 of 13 animals [Hamir et al. 2001]). This
finding raised concerns that CWD prions might be transmitted to cattle grazing
in contaminated pastures."
Please see ;
Within 26 months post inoculation, 12 inoculated animals had lost weight,
revealed abnormal clinical signs, and were euthanatized. Laboratory tests
revealed the presence of a unique pattern of the disease agent in tissues of
these animals. These findings demonstrate that when CWD is directly inoculated
into the brain of cattle, 86% of inoculated cattle develop clinical signs of the
disease.
" although the infection rate was low (4 of 13 animals [Hamir et al.
2001]). "
shouldn't this be corrected, 86% is NOT a low rate. ...
kindest regards,
Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518
Thank you!
Thanks so much for your updates/comments. We intend to publish as rapidly
as possible all updates/comments that contribute substantially to the topic
under discussion.
re-Prions David W. Colby1,* and Stanley B. Prusiner1,2 + Author
Affiliations
1Institute for Neurodegenerative Diseases, University of California, San
Francisco, San Francisco, California 94143 2Department of Neurology, University
of California, San Francisco, San Francisco, California 94143 Correspondence:
stanley@ind.ucsf.edu
Mule deer, white-tailed deer, and elk have been reported to develop CWD. As
the only prion disease identified in free-ranging animals, CWD appears to be far
more communicable than other forms of prion disease. CWD was first described in
1967 and was reported to be a spongiform encephalopathy in 1978 on the basis of
histopathology of the brain. Originally detected in the American West, CWD has
spread across much of North America and has been reported also in South Korea.
In captive populations, up to 90% of mule deer have been reported to be positive
for prions (Williams and Young 1980). The incidence of CWD in cervids living in
the wild has been estimated to be as high as 15% (Miller et al. 2000). The
development of transgenic (Tg) mice expressing cervid PrP, and thus susceptible
to CWD, has enhanced detection of CWD and the estimation of prion titers
(Browning et al. 2004; Tamgüney et al. 2006). Shedding of prions in the feces,
even in presymptomatic deer, has been identified as a likely source of infection
for these grazing animals (Williams and Miller 2002; Tamgüney et al. 2009b). CWD
has been transmitted to cattle after intracerebral inoculation, although the
infection rate was low (4 of 13 animals [Hamir et al. 2001]). This finding
raised concerns that CWD prions might be transmitted to cattle grazing in
contaminated pastures.
snip...
----- Original Message -----
From: David Colby To: flounder9@verizon.net
Cc: stanley@XXXXXXXX
Sent: Tuesday, March 01, 2011 8:25 AM
Subject: Re: FW: re-Prions David W. Colby1,* and Stanley B. Prusiner1,2 +
Author Affiliations
Dear Terry Singeltary,
Thank you for your correspondence regarding the review article Stanley
Prusiner and I recently wrote for Cold Spring Harbor Perspectives. Dr. Prusiner
asked that I reply to your message due to his busy schedule. We agree that the
transmission of CWD prions to beef livestock would be a troubling development
and assessing that risk is important. In our article, we cite a peer-reviewed
publication reporting confirmed cases of laboratory transmission based on
stringent criteria. The less stringent criteria for transmission described in
the abstract you refer to lead to the discrepancy between your numbers and ours
and thus the interpretation of the transmission rate. We stand by our assessment
of the literature--namely that the transmission rate of CWD to bovines appears
relatively low, but we recognize that even a low transmission rate could have
important implications for public health and we thank you for bringing attention
to this matter.
Warm Regards, David Colby -- David Colby, PhD
Assistant Professor Department of Chemical Engineering University of
Delaware
===========END...TSS==============
SNIP...SEE FULL TEXT ;
Chronic Wasting Disease Q&A from St. Joseph MO MDC meeting claimed
;
>>> no risk for humans to cwd ?
NOW, let’s take a look at what the science is saying on the risk factors of
human TSE prion disease from CWD prion disease of cervids.
first, from the cdc/nih et al prion gods, and what they said on human cwd
potential, and what that might look like ;
now, let’s see what the authors said about this casual link, personal
communications years ago. see where it is stated NO STRONG evidence. so, does
this mean there IS casual evidence ????
“Our conclusion stating that we found no strong evidence of CWD
transmission to humans”
From: TSS (216-119-163-189.ipset45.wt.net)
Subject: CWD aka MAD DEER/ELK TO HUMANS ???
Date: September 30, 2002 at 7:06 am PST
From: "Belay, Ermias"
To:
Cc: "Race, Richard (NIH)" ; ; "Belay, Ermias"
Sent: Monday, September 30, 2002 9:22 AM
Subject: RE: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
Dear Sir/Madam,
In the Archives of Neurology you quoted (the abstract of which was attached
to your email), we did not say CWD in humans will present like variant
CJD.
That assumption would be wrong. I encourage you to read the whole article
and call me if you have questions or need more clarification (phone:
404-639-3091). Also, we do not claim that "no-one has ever been infected with
prion disease from eating venison." Our conclusion stating that we found no
strong evidence of CWD transmission to humans in the article you quoted or in
any other forum is limited to the patients we investigated.
Ermias Belay, M.D. Centers for Disease Control and Prevention
-----Original Message-----
From:
Sent: Sunday, September 29, 2002 10:15 AM
To: rr26k@nih.gov; rrace@niaid.nih.gov; ebb8@CDC.GOV
Subject: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
Sunday, November 10, 2002 6:26 PM ......snip........end..............TSS
Thursday, April 03, 2008
A prion disease of cervids: Chronic wasting disease
2008 1: Vet Res. 2008 Apr 3;39(4):41
A prion disease of cervids: Chronic wasting disease
Sigurdson CJ.
snip...
*** twenty-seven CJD patients who regularly consumed venison were reported
to the Surveillance Center***,
snip...
full text ;
Monday, February 09, 2009
Exotic Meats USA Announces Urgent Statewide Recall of Elk Tenderloin
Because It May Contain Meat Derived From An Elk Confirmed To Have CWD
snip...
Cross-sequence transmission of sporadic Creutzfeldt-Jakob disease creates
a new prion strain
Date: August 25, 2007 at 12:42 pm PST
our results raise the possibility that CJD cases classified as VV1 may
include cases caused by iatrogenic transmission of sCJD-MM1 prions or food-borne
infection by type 1 prions from animals, e.g., chronic wasting disease prions in
cervid. In fact, two CJD-VV1 patients who hunted deer or consumed venison have
been reported (40, 41). The results of the present study emphasize the need for
traceback studies and careful re-examination of the biochemical properties of
sCJD-VV1 prions.
Wednesday, March 18, 2009
Noah's Ark Holding, LLC, Dawson, MN RECALL Elk products contain meat
derived from an elk confirmed to have CWD NV, CA, TX, CO, NY, UT, FL, OK RECALLS
AND FIELD CORRECTIONS: FOODS CLASS II
CWD TO HUMAN RISK FACTORS PRION2013
PRION2013 CONGRESSIONAL ABSTRACTS
HD.13: CWD infection in the spleen of humanized transgenic mice
Liuting Qing and Qingzhong Kong
Case Western Reserve University; Cleveland, OH USA
Chronic wasting disease (CWD) is a widespread prion disease in free-ranging
and captive cervid species in North America, and there is evidence suggesting
the existence of multiple CWD strains. The susceptibility of human CNS and
peripheral organs to the various CWD prion strains remains largely unclear.
Current literature suggests that the classical CWD strain is unlikely to infect
human brain, but the potential for peripheral infection by CWD in humans is
unknown. We detected protease-resistant PrpSc in the spleens of a few humanized
transgenic mice that were intracerebrally inoculated with natural CWD isolates,
but PrpSc was not detected in the brains of any of the CWD-inoculated mice. Our
ongoing bioassays in humanized Tg mice indicate that intracerebral challenge
with such PrpSc-positive humanized mouse spleen already led to prion disease in
most animals. ***These results indicate that the CWD prion may have the
potential to infect human peripheral lymphoid tissues.
=====
Oral.15: Molecular barriers to zoonotic prion transmission: Comparison of
the ability of sheep, cattle and deer prion disease isolates to convert normal
human prion protein to its pathological isoform in a cell-free system
Marcelo A.Barria,1 Aru Balachandran,2 Masanori Morita,3 Tetsuyuki
Kitamoto,4 Rona Barron,5 Jean Manson,5 Richard Kniqht,1 James W. lronside1 and
Mark W. Head1
1National CJD Research and Surveillance Unit; Centre for Clinical Brain
Sciences; School of Clinical Sciences; The University of Edinburgh; Edinburgh,
UK; 2National and OIE Reference Laboratory for Scrapie and CWD; Canadian Food
Inspection Agency; Ottawa Laboratory; Fallowfield. ON Canada; 3Infectious
Pathogen Research Section; Central Research Laboratory; Japan Blood Products
Organization; Kobe, Japan; 4Department of Neurological Science; Tohoku
University Graduate School of Medicine; Sendai. Japan; 5Neurobiology Division;
The Roslin Institute and R(D)SVS; University of Edinburgh; Easter Bush;
Midlothian; Edinburgh, UK
Background. Bovine spongiform encephalopathy (BSE) is a known zoonotic
prion disease, resulting in variant Creurzfeldt- Jakob disease (vCJD) in humans.
In contrast, classical scrapie in sheep is thought to offer little or no danger
to human health. However, a widening range of prion diseases have been
recognized in cattle, sheep and deer. The risks posed by individual animal prion
diseases to human health cannot be determined a priori and are difficult to
assess empirically. The fundamemal event in prion disease pathogenesis is
thought to be the seeded conversion of normal prion protein (PrPC) to its
pathological isoform (PrPSc). Here we report the use of a rapid molecular
conversion assay to test whether brain specimens from different animal prion
diseases are capable of seeding the conversion of human PrPC ro PrPSc.
Material and Methods. Classical BSE (C-type BSE), H-type BSE, L-type BSE,
classical scrapie, atypical scrapie, chronic wasting disease and vCJD brain
homogenates were tested for their ability to seed conversion of human PrPC to
PrPSc in protein misfolding cyclic amplification (PMCA) reactions. Newly formed
human PrPSc was detected by protease digestion and western blotting using the
antibody 3F4.
Results. C-type BSE and vCJD were found to efficiently convert PrPC to
PrPSc. Scrapie failed to convert human PrPC to PrPSc. Of the other animal prion
diseases tested only chronic wasting disease appeared to have the capability ro
convert human PrPC to PrPSc. The results were consistent whether the human PrPC
came from human brain, humanised transgenic mouse brain or from cultured human
cells and the effect was more pronounced for PrPC with methionine at codon 129
compared with that with valine.
Conclusion. Our results show that none of the tested animal prion disease
isolates are as efficient as C-type BSE and vCJD in converting human prion
protein in this in vitro assay. ***However, they also show that there is no
absolute barrier ro conversion of human prion protein in the case of chronic
wasting disease.
=====
Invited.16: Studies of chronic wasting disease transmission in cervid and
non-cervid species
Edward A, Hoover,1 Candace K. Mathiason,1 Davin M. Henderson,1 Nicholas J.
Haley,1 Davis M. Seelig,1 Nathaniel D. Denkers,1 Amy V. Nalls,1 Mark D. Zabe,1
Glenn C. Telling,1 Fernando Goni2 and Thomas Wisniewski,2
1Prion Research Center; Colorado State University; Fort Collins, CO USA;
2New York University School of Medicine; New York, NY USA
How and why some misfolded proteins become horizontally transmitted agents
and occasionally cross species barriers are issues fundamental to understanding
prion disease. Chronic wasting disease (CWD) of cervids is perhaps a prototype
of horizontal prion transmission, encompassing efficient mucosal uptake,
lymphoid amplification, neuroinvasion, peripheralization, and dissemination via
mucosal excretion. Efficient mucosal transmission of CWD in deer has been
demonstrated by oral, nasal, aerosol, and indirect contact exposure. In
addition, other studies (Mathiason CK, et al.) reported at the symposium support
a significant role for pre- and/or postnatal transmission of CWD from doe to
offspring. Accumulating, yet still incomplete, evidence also suggests that the
period of relatively covert CWD infection may be longer than originally thought.
Given the above, minimally invasive sensitive assays based on body fluids from
live animals would aid substantially in understanding the biology of CWD. We
have been applying seeded realtirne quaking-induced amplification of recombinant
PrP substrates (i.e., RT-QuIC methodology) to: (1) investigate antemortem CWD
detection, and (2) model PrP-based species barriers and trans-species
adaptation-topics we previously explored using sPMCA and in vivo bioassays. At
this symposium, we report sensitive and specific detection CWD prions in saliva,
urine, blood (Mathiason lab), and rectal and pharyngeal lymph node samples
(Haley NJ, et al.) from pre-symptomatic and symptomatic experimentally and
naturally exposed deer. Other ongoing studies are employing RT-QuIC methodology
to model amplification barriers among CWD, FSE, BSE, and CJD prions using
cervine, feline, bovine, human, and promiscuous rPrP substrates and the above
species prion seeds, cellular co-factors, and transgenic mice. Finally, in
collaboration with the Wisniewski laboratory, we are conducting of experimental
CWD vaccination studies in deer employing oral administration of an attenuated
Salmonella vector expressing cervid PrP epitopes.
=====
AD.06: Detecting prions in the brain and blood of TSE-infected deer and
hamsters
Alan Elder,1 Davin Henderson,1 Anca Selariu,1 Amy Nalls,1 Byron Caughey,2
Richard Bessen,1 Jason Bartz3 and Candace Mathiason1
1Colorado State University; Fort Collins, CO USA; 2NIH Rocky Mountain
Laboratories; Hamilton, MT USA; 3Creighton University; Omaha, NE USA
While large quantities of protease resistant prion protein (PrPres) can be
demonstrated by western blot or IHC in lymphoid biopsies or post-mortem brain
tissues harvested from prion-infected animals, these conventional assays are
less reliable as means to detect the small quantities of prions thought to be
present in bodily fluids or associated with early and asymptomatic phases of TSE
disease. The Real Time-Quaking Induced Conversion (RT-QuIC) assay is capable of
detecting prions at concentrations below the level of sensitivity of
conventional assays and provides a real-time fluorescent readout negating the
use of proteases. We have made modifications to the RT-QuIC assay to utilize it
for the detection of PrPres in brain and blood harvested from various species
infected with prions. In this study, we analyzed CWD-infected deer and
CWD/TME-infected hamster whole blood to determine the effect of:
(1) various anticoagulants,
(2) freezing and
(3) NaPTA precipitation.
Brain tissue and blood collected from naive deer and hamsters served as
negative controls.
We were able to demonstrate amplifiable prions in
(1) brain and blood samples harvested from CWD/TME-infected animals,
(2) heparinized blood,
(3) frozen vs. fresh blood and
(4) NaPTA treated samples.
The RT-QuIC assay is able to detect PrPres in various species of animals
and shows promise as an antemortem diagnostic tool for blood-borne TSEs.
=====
Sunday, July 21, 2013
*** As Chronic Wasting Disease CWD rises in deer herd, what about risk for
humans?
sCJDMM1-2 should be considered as a separate entity at this time.
All of the Heidenhain variants were of the methionine/ methionine type 1
molecular subtype.
*** The potential impact of prion diseases on human health was greatly
magnified by the recognition that interspecies transfer of BSE to humans by beef
ingestion resulted in vCJD. While changes in animal feed constituents and
slaughter practices appear to have curtailed vCJD, there is concern that CWD of
free-ranging deer and elk in the U.S. might also cross the species barrier.
Thus, consuming venison could be a source of human prion disease. Whether BSE
and CWD represent interspecies scrapie transfer or are newly arisen prion
diseases is unknown. Therefore, the possibility of transmission of prion disease
through other food animals cannot be ruled out. There is evidence that vCJD can
be transmitted through blood transfusion. There is likely a pool of unknown size
of asymptomatic individuals infected with vCJD, and there may be asymptomatic
individuals infected with the CWD equivalent. These circumstances represent a
potential threat to blood, blood products, and plasma supplies.
Friday, September 27, 2013
Uptake of Prions into Plants
Presentation Abstract
SEE MORE ;
Sunday, August 25, 2013
***Prion2013 Chronic Wasting Disease CWD risk factors, humans, domestic
cats, blood, and mother to offspring transmission
Friday, August 09, 2013
***CWD TSE prion, plants, vegetables, and the potential for environmental
contamination
Thursday, August 08, 2013
***Characterization of the first case of naturally occurring chronic
wasting disease in a captive red deer (Cervus elaphus) in North America
Sunday, September 01, 2013
***hunting over gut piles and CWD TSE prion disease
Wednesday, September 04, 2013
***cwd - cervid captive livestock escapes, loose and on the run in the
wild...
Tuesday, September 10, 2013
***Review and Updates of the USDA-APHIS Veterinary Services (VS) National
Chronice Wasting Disease (CWD) Program 2012-2013
Tuesday, September 17, 2013
***USAHA 116TH ANNUAL MEETING October 18 – 24, 2012 CWD, Scrapie, BSE, TSE
prion (September 17, 2013)
Friday, November 09, 2012
*** Chronic Wasting Disease CWD in cervidae and transmission to other
species
Sunday, November 11, 2012
*** Susceptibilities of Nonhuman Primates to Chronic Wasting Disease
November 2012
Friday, December 14, 2012
***Susceptibility Chronic Wasting Disease (CWD) in wild cervids to Humans
2005 - December 14, 2012
Sunday, June 09, 2013
***Missouri House forms 13-member Interim Committee on the Cause and Spread
of Chronic Wasting Disease CWD
Sunday, August 11, 2013
Creutzfeldt-Jakob Disease CJD cases rising North America updated report
August 2013
*** Creutzfeldt-Jakob Disease CJD cases rising North America with Canada
seeing an extreme increase of 48% between 2008 and 2010
Thursday, September 26, 2013
***Minimise transmission risk of CJD and vCJD in healthcare settings
Guidance
Chronic Wasting Disease Q&A from St. Joseph MO MDC meeting claimed
;
>>>cwd no risk factor from the world of insects
Subject: Transmission of TSEs through ectoparasites i.e. P. tenuis and CWD
Date: May 3, 2007 at 9:05 am PST
CONFIDENTIAL SEAC 97/2 Annex 2 UNITED KINGDOM ACCREDITATION SERVICE (UKAS)
ASSESSMENT REPORT
Other organisms
Transmission of TSEs through ectoparasites has been postulated by Lupi5.
Post et al6 fed larvae of meat eating and myiasis causing flies with brain
material from scrapieinfected hamsters. Two days after eating infected material,
the larvae showed high amounts of PrPSc by Western blot. In further studies, the
inner organs of larvae, which had been fed with scrapie brain, were extracted
and fed to hamsters. Six out of eight hamsters developed scrapie. Two out of
four hamsters fed on scrapie infected pupae subsequently developed scrapie.
I AGAIN raise the possibility of that damn brain eating worm in elk and CWD
transmission via elk, deer, and other critters eating that worm. ...tss
Immunodiagnosis of experimental Parelaphostrongylus tenuis infection in elk
Oladele Ogunremi, Murray Lankester, and Alvin Gajadhar Centre for Animal
Parasitology, Canadian Food Inspection Agency, 116 Veterinary Road, Saskatoon,
Saskatchewan S7N 2R3 (Ogunremi, Gajadhar); Department of Biology, Lakehead
University, 955 Oliver Road, Thunder Bay, Ontario P7B 5E1 (Lankester).
Elk infected with the meningeal worm, Parelaphostrongylus tenuis
(Protostrongylidae), do not consistently excrete larvae in feces, making the
current method of diagnosing live animals using the Baermann fecal technique
unreliable. Serological diagnosis could prove more useful in diagnosing
field-infected animals but depends on the identification and availability of
good quality antigen. To mimic field infections, 2 elk were inoculated with 6
infective L3 larvae of P. tenuis, and another 2 with 20 L3 larvae. Fecal samples
were examined for nematode larvae using the Baermann technique and serum samples
taken were tested for anti-P. tenuis antibody with ELISAs by using the
excretory-secretory (ES) products of L3, and sonicated adult worms as antigens.
One animal passed first-stage larvae in its feces 202 days postinoculation, but
passed none thereafter. The remaining 3 inoculated animals did not pass larvae.
In contrast to parasite detection, antibodies against larval ES products were
detected in all animals starting from 14 to 28 days postinoculation and
persisted until the termination of the experiment on day 243 in 2 animals that
harbored adult worms. Antibodies against somatic antigens of the adult worm were
not detected until day 56 but also persisted until the end of the experiment in
the animals with adult worms. In 2 elk that had no adult worms at necropsy,
anti-ES antibodies were detected transiently in both, while anti-adult worm
antibodies were present transiently in one. These findings confirm the
superiority of P. tenuis larval ES products over somatic adult worm antigens as
serodiagnostic antigens, as previously observed in studies of infected
white-tailed deer, and extend the application of the newly developed ELISA test
in diagnosing and monitoring cervids experimentally infected with P. tenuis.
Subject: TSE & insects as a vector of potential transmission
Date: October 26, 2006 at 12:50 pm PST
i try to keep an open mind about any other routes and sources that we may
be overlooking. i mean, there is enough TSE protein in circulation now VIA the
FDA, just in 2006 alone, and the oral route has been proven with BSE, and the
non-forced oral consumption of scrapie to primate, as to not worry about a
natural route of a few worms that have maybe been feasting on a deer that's
brain is infected with CWD, then excreted out, and then passed on to another
worm hungry deer looking for that feast. i suppose maybe just another potential
route and source for a TSE, and possibly even a 'double dose' so to speak from
not only the worm in the feces (maybe triple with feces), but the soil as well
(see soil and prion study as well below) following that are some other studies
that may be of interest ;
Myiasis as a risk factor for prion diseases in humans
Journal of the European Academy of Dermatology and Venereology Volume 20
Page 1037 - October 2006 doi:10.1111/j.1468-3083.2006.01595.x Volume 20 Issue 9
REVIEW ARTICLE Myiasis as a risk factor for prion diseases in humans O
Lupi *
Abstract
Prion diseases are transmissible spongiform encephalopathies of humans and
animals. The oral route is clearly associated with some prion diseases,
according to the dissemination of bovine spongiform encephalopathy (BSE or mad
cow disease) in cattle and kuru in humans. However, other prion diseases such as
scrapie (in sheep) and chronic wasting disease (CWD) (in cervids) cannot be
explained in this way and are probably more associated with a pattern of
horizontal transmission in both domestic and wild animals. The skin and mucous
membranes are a potential target for prion infections because keratinocytes and
lymphocytes are susceptible to the abnormal infective isoform of the prion
protein. Iatrogenic transmission of Creutzfeldt–Jakob disease (CJD) was also
recognized after corneal transplants in humans and scrapie was successfully
transmitted to mice after ocular instillation of infected brain tissue,
confirming that these new routes could also be important in prion infections.
Some ectoparasites have been proven to harbour prion rods in laboratory
experiments. Prion rods were identified in both fly larvae and pupae; adult
flies are also able to express prion proteins. The most common causes of myiasis
in cattle and sheep, closely related animals with previous prion infections, are
Hypoderma bovis and Oestrus ovis, respectively. Both species of flies present a
life cycle very different from human myiasis, as they have a long contact with
neurological structures, such as spinal canal and epidural fat, which are
potentially rich in prion rods. Ophthalmomyiases in humans is commonly caused by
both species of fly larvae worldwide, providing almost direct contact with the
central nervous system (CNS). The high expression of the prion protein on the
skin and mucosa and the severity of the inflammatory response to the larvae
could readily increase the efficiency of transmission of prions in both animals
and humans.
International Journal of Dermatology Volume 42 Page 425 - June 2003
doi:10.1046/j.1365-4362.2003.00345.x Volume 42 Issue 6
Review Could ectoparasites act as vectors for prion diseases? Omar Lupi,
MD, PhD Abstract
Prion diseases are rare neurodegenerative diseases of humans and animals
with a lethal evolution. Several cell types found on the human skin, including
keratinocytes, fibroblasts and lymphocytes, are susceptible to the abnormal
infective isoform of the prion protein, which transforms the skin to produce a
potential target for prion infection. Iatrogenic transmission of
Creutzfeldt-Jakob disease was also recognized after corneal transplants in
humans, and scrapie was successfully transmitted to mice after ocular
instillation of infected brain tissue, confirming that these new routes, as well
as cerebral inoculation and oral ingestion, could be important in prion
infections. Animal prion infections, such as scrapie (sheep) and "mad cow
disease" (cattle), have shown a pattern of horizontal transmission in farm
conditions and several ectoparasites have been shown to harbor prion rods in
laboratory experiments. Fly larvae and mites were exposed to brain-infected
material and were readily able to transmit scrapie to hamsters. New lines of
evidence have confirmed that adult flies are also able to express prion
proteins. Because ocular and cerebral myiases and mite infestation are not rare
worldwide, and most cases are caused by fly larvae or hay mites that usually
affect sheep and cattle, it is important to discuss the possibility that these
ectoparasites could eventually act as reservoirs and/or vectors for prion
diseases.
P. tenuis – The White-tailed Deer Parasite
“Brain worms” (meningeal worms) can affect sheep, goats, llamas, alpacas,
moose and other exotic small ruminants
M. Kopcha, D.V.M., M.S., J. S. Rook, D.V.M. & D. Hostetler, D.V.M
MSU Extension & Ag. Experiment Station
Michigan State University
College of Veterinary Medicine
Many livestock producers are familiar with internal parasites that invade
the digestive system (the abomasum, small or large intestines), liver, and
lungs. An internal parasite which may not be so well-recognized is one that
invades the central nervous system (brain and spinal cord). Commonly called the
“brain worm” or meningeal worm (the meninges are a thin membrane that covers the
brain and spinal column), the scientific name for this parasite is
Parelaphostroneylus tenuis (P. tenuis), and its natural host is the White-tailed
deer. Usually, P. tenuis completes its life cycle in the deer (Figure 1) without
causing noticeable problems. ***However, when P. tenuis is ingested by
unnatural, or aberrant hosts such as, llamas, sheep, goats, moose, elk, caribou,
and other susceptible ruminants, the parasite moves into the brain and/or spinal
cord, damaging delicate nervous tissue.
Neurologic problems result.
White-tailed deer may he parasitized by P. tenuis year-round. However, the
neurologic disease seen in aberrant hosts has a seasonal occurrence that starts
in the late summer and continues until a hard freeze occurs. A cool, moist
summer and/or a mild winter may extend the period during which the disease
occurs.
How does it occur?
To understand this disease and how to prevent or minimize its occurrence,
it is important to understand the life cycle of P. tenuis in the White-tailed
deer and what happens when the parasite is ingested by susceptible ruminants.
The life cycle is as follows (Figure 1): adult meningeal worms live in the
deer's central nervous system (brain and spinal cord) and produce eggs which
hatch into larvae. The larvae migrate from the deer's central nervous system to
the lungs, where they are coughed into the mouth, swallowed and passed from the
intestinal tract with the manure. This portion of the life cycle takes
approximately three months (Figure 1 - numbers 1 and 2).
After excreted in the manure, larvae must continue their development in an
intermediate host (certain land-dwelling snails and slugs) for another three to
four weeks until they reach their infective stage (Figure 1 - numbers 3 and 4).
White-tailed deer become infested with P. tenuis by eating these snails or
slugs that contain the infective stage of the larvae (Figure 1 - number 5). Once
ingested, the larvae migrate through the deer’s gut and eventually move into
their central nervous system where they mature into adults, produce eggs, Figure
2 The Angora goat in the center of the picture had a mild lameness in its left
forelimb (arrow). The presumptive diagnosis was meningeal worm infestation. Mild
cases such as this one may recover spontaneously.
snip...
other potential vectors for cwd tse prion disease ;
Wednesday, October 17, 2012
Prion Remains Infectious after Passage through Digestive System of American
Crows (Corvus brachyrhynchos)
Sunday, November 01, 2009
AS THE CROW FLIES, SO DOES CWD
American crows (Corvus brachyrhynchos) and potential spreading of CWD
through feces of digested infectious carcases
Monday, July 13, 2009
Deer Carcass Decomposition and Potential Scavenger Exposure to Chronic
Wasting Disease
Sunday, July 07, 2013
Could avian scavengers translocate infectious prions to disease-free areas
initiating new foci of chronic wasting disease?
Prion. 2013 Jul 3;7(4). [Epub ahead of print]
another fine example letter. this one will floor you. 'Jimmy crack corn,
and they don't care' no big deal, just flush those mixers with corn, then feed
the corn to the deer. NOooooo problem.
Subject: ''MORE'' 'VIOLATORS' of Animal Proteins Prohibited in Ruminant
Feed--U.S.A. (more and more MAD COW FEED RULES BROKEN IN U.S.A.]
Date: Tue, 24 Apr 2001 09:45:15 –0700
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy
To: BSE-L@uni-karlsruhe.de References: 1 , 2
######### Bovine Spongiform Encephalopathy #########
Greetings again List Members,
''MORE'' violations and warning letters over FDA MAD COW feed ban
regulations that have not been complied with since the Aug. 4, 1997 'partial'
feed ban was implemented...
they implemented something, then forgot to enforce it $$$$$
another fine example letter. this one will floor you. 'Jimmy crack corn,
and they don't care' no big deal, just flush those mixers with corn, then feed
the corn to the deer. NOooooo problem.
these people must be brain dead???
DEPARTMENT OF HEALTH & HUMAN SERVICES PUBLIC HEALTH SERVICE FOOD AND
DRUG ADMINISTRATION
April 9, 2001 WARNING LETTER
01-PHI-12 CERTIFIED MAIL RETURN RECEIPT REQUESTED
Brian J. Raymond, Owner Sandy Lake Mills 26 Mill Street P.O. Box 117 Sandy
Lake, PA 16145 PHILADELPHIA DISTRICT
Tel: 215-597-4390
Dear Mr. Raymond:
Food and Drug Administration Investigator Gregory E. Beichner conducted an
inspection of your animal feed manufacturing operation, located in Sandy Lake,
Pennsylvania, on March 23, 2001, and determined that your firm manufactures
animal feeds including feeds containing prohibited materials. The inspection
found significant deviations from the requirements set forth in Title 21, code
of Federal Regulations, part 589.2000 - Animal Proteins Prohibited in Ruminant
Feed. The regulation is intended to prevent the establishment and amplification
of Bovine Spongiform Encephalopathy (BSE) . Such deviations cause products being
manufactured at this facility to be misbranded within the meaning of Section
403(f), of the Federal Food, Drug, and Cosmetic Act (the Act).
Our investigation found failure to label your swine feed with the required
cautionary statement "Do Not Feed to cattle or other Ruminants" The FDA suggests
that the statement be distinguished by different type-size or color or other
means of highlighting the statement so that it is easily noticed by a purchaser.
In addition, we note that you are using approximately 140 pounds of cracked
corn to flush your mixer used in the manufacture of animal feeds containing
prohibited material. This flushed material is fed to wild game including deer, a
ruminant animal. Feed material which may potentially contain prohibited material
should not be fed to ruminant animals which may become part of the food chain.
The above is not intended to be an all-inclusive list of deviations from
the regulations. As a manufacturer of materials intended for animal feed use,
you are responsible for assuring that your overall operation and the products
you manufacture and distribute are in compliance with the law. We have enclosed
a copy of FDA's Small Entity Compliance Guide to assist you with complying with
the regulation... blah, blah, blah...
-------- Original Message --------
Subject: MAD DEER FEED BAN WARNING LETTER RECALL 6 TONS DISTRIBUTED
USA
Date: Wed, 20 Oct 2004 14:53:56 –0500
From: "Terry S. Singeltary Sr." flounder@WT.NET
Reply-To: Bovine Spongiform Encephalopathy BSE-L@UNI-KARLSRUHE.DE
To: BSE-L@UNI-KARLSRUHE.DE
##################### Bovine Spongiform Encephalopathy
#####################
PRODUCT
Product is __custom made deer feed__ packaged in 100 lb. poly bags. The
product has no labeling. Recall # V-003-5.
CODE
The product has no lot code. All custom made feed purchased between June
24, 2004 and September 8, 2004.
RECALLING FIRM/MANUFACTURER
Farmers Elevator Co, Houston, OH, by telephone and letter dated September
27, 2004. Firm initiated recall is ongoing.
REASON
Feed may contain protein derived from mammalian tissues which is prohibited
in ruminant feed.
VOLUME OF PRODUCT IN COMMERCE
Approximately 6 tons.
DISTRIBUTION OH.
END OF ENFORCEMENT REPORT FOR October 20, 2004
################# BSE-L-subscribe-request@uni-karlsruhe.de
#################
now, just what is in that deer feed? _ANIMAL PROTEIN_
Subject: MAD DEER/ELK DISEASE AND POTENTIAL SOURCES
Date: Sat, 25 May 2002 18:41:46 –0700
From: "Terry S. Singeltary Sr."
Reply-To: BSE-L
To: BSE-L
8420-20.5% Antler Developer For Deer and Game in the wild Guaranteed
Analysis Ingredients / Products Feeding Directions
snip...
_animal protein_
REFERENCES
snip...see full text ;
-------- Original Message --------
Subject: DOCKET-- 03D-0186 -- FDA Issues Draft Guidance on Use of Material
From Deer and Elk in Animal Feed; Availability
Date: Fri, 16 May 2003 11:47:37 –0500
From: "Terry S. Singeltary Sr." To: fdadockets@oc.fda.gov
Greetings FDA,
i would kindly like to comment on;
Docket 03D-0186
FDA Issues Draft Guidance on Use of Material From Deer and Elk in Animal
Feed; Availability
PO-248: TSE infectivity survives burial for five years with little
reduction in titer
Allister Smith, Robert Somerville, Karen Fernie The Roslin Institute and
R(D)SVS; University of Edinburgh; Edinburgh, UK
BSE infected animals, BSE-contaminated materials and other sources of TSE
(prion) infection, such as carcasses from scrapie infected sheep, CWD infected
deer and cadavers of individuals infected with CJD may all end up in the
environment through burial or other methods of disposal. They may continue to
act as a reservoir of TSE infectivity if cattle or other susceptible animals
were to be exposed to these sources in the future. In order to address these
concerns, we performed two large scale demonstration experiments under field
conditions which were designed to mimic some of the ways by which TSE infected
materials may have been disposed of. The project examined the fate of TSE
infectivity over a period of five years in two scenarios; when the infectivity
was contained within bovine heads and when the infectivity was buried without
any containment. Two soil types were compared: a sandy loam and a clay loam. We
used the 301V TSE strain which was derived by serial passage of BSE in VM mice.
TSE infectivity was recovered from all the heads exhumed annually for five
years from both types of soil, with little reduction in the amount of
infectivity throughout the period of the experiment. Small amounts of
infectivity were found in the soil immediately surrounding the heads, but not in
samples remote from them. Similarly there was no evidence of significant lateral
movement of infectivity from the buried bolus. However large amounts of TSE
infectivity were recovered at the site of burial of both boluses. There was
limited vertical upward movement of infectivity from the bolus buried in clay
soil and downward movement from the bolus buried in sandy soil.
Now that these experiments are completed we conclude that TSE infectivity
is likely to survive burial for long periods of time with minimal loss of
infectivity and restricted movement from the site of burial. These experiments
emphasize that the environment is a viable reservoir for retaining large
quantities of TSE infectivity, and reinforce the importance of risk assessment
when disposing of this type of infectious material.
see more about soil content and CWD here ;
Friday, February 25, 2011
Soil clay content underlies prion infection odds Soil clay content
underlies prion infection odds
Saturday, March 10, 2012
CWD, GAME FARMS, urine, feces, soil, lichens, and banned mad cow protein
feed CUSTOM MADE for deer and elk
Thursday, May 31, 2012
CHRONIC WASTING DISEASE CWD PRION2012 Aerosol, Inhalation transmission,
Scrapie, cats, species barrier, burial, and more
Friday, February 08, 2013
*** Behavior of Prions in the Environment: Implications for Prion Biology
Greetings again Missouri et al,
considering what we have learned about environmental factors, and soil
factors of the TSE prion disease with CWD and Scrapie, and other transmission
studies in many different species, the new more sensitive TSE prion testing
techniques (I am very interested in the atypical BSE strains), as the crows fly
and TSE there from, I think we cannot rule the possibility of insects and or the
ingestion of insects, that may have been exposed to the TSE prion, that this
could be a potential vector of the TSE prion disease. cervids are highly
susceptible to oral consumption of the TSE prion disease. whether or not the
insect becomes diseased is one thing, but as an instrument of transmission
feasting on the brain of a CWD infected cervid, and then consumed by a cervid,
or whatever, then this is a real potential vector of transmission. reminds me of
the decades old argument of feeding ruminant by-product to fowl or porcine, on
the false assumption that the fowl or porcine will not go down with a TSE (which
tse prion disease has been proven to transmit to both fowl and porcine, but
that’s another day for debate), but the fact on that false assumption, even
though, the pigs and or chicken would consume the tainted TSE prion product and
even though it may not go clinical with TSE prion disease, even though, the said
potential banned TSE prion ruminant protein in feed would survive the digestive
tract, thus using said by-products from the fowl or porcine would still be
exposed via said potential banned by-products in the digestive tract.Gibbs et
al. then you must factor in whether the one dose theory or the accumulation
theory, or both (because you have to figure in genetic susceptibility from both
ends) , for when a TSE prion disease goes from sub-clincal to clinical disease,
or if it will, can ever be proven, only then will these assumptions be proven
correct or incorrect. but this continued gamble on if’s and what not’s,
potential, could be, might be, might not’s and never’s, today in 2013, so many
humans and animals exposed, and when the incubation period hits it’s peak from
the highest point of load factors from all the TSEs’ in North America, then you
have to hedge your bet with all the failures of the i.e. FDA/USDA/OIE TRIPLE
FIREWALLS of proven deceit and fraud over the past 3 decades or so with the many
different Transmissible Spongiform Encephalopathy’s TSE aka mad cow type prion
disease in the many different species in the USA and North America, the consumer
consumption via food, and other products, and the many different iatrogenic
potentials there from, only time will tell. but to avoid considering any of
these factors until proven otherwise, would not be scientific. . ...if your not
confused now, that’s great, because I think I confused myself pondering out loud
here. ...
kind regards, terry
LAYPERSON!
Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518
flounder9@verizon.net
posted by Terry S. Singeltary Sr. at
5:02 PM
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