Progressive accumulation of the abnormal conformer of the prion protein and spongiform encephalopathy in the obex of nonsymptomatic and symptomatic Rocky Mountain elk (Cervus elaphus nelsoni) with chronic wasting disease
Progressive accumulation of the abnormal conformer of the prion protein and
spongiform encephalopathy in the obex of nonsymptomatic and symptomatic Rocky
Mountain elk (Cervus elaphus nelsoni) with chronic wasting disease
Terry R. Spraker1 Thomas Gidlewski Jenny G. Powers Tracy Nichols Aru
Balachandran Bruce Cummings Margaret A. Wild Kurt VerCauteren Katherine I.
O’Rourke Colorado State University Diagnostic Laboratory, College of Veterinary
Medicine and Biomedical Sciences, Colorado State University, Fort Collins, CO
(Spraker, Cummings) National Wildlife Research Center, U.S. Department of
Agriculture (USDA), Animal and Plant Health Inspection Service, Wildlife
Services, Fort Collins, CO (Gidlewski, Nichols, VerCauteren) National Park
Service, Biological Resources Management Division, Fort Collins, CO (Powers,
Wild) Canadian Food Inspection Services, Ottawa, Ontario, Canada (Balachandran)
USDA, Agricultural Research Service, Pullman, WA (O’Rourke) ↵1Terry R. Spraker,
Colorado State University Diagnostic Laboratory, College of Veterinary Medicine
and Biomedical Sciences, Colorado State University, Fort Collins CO 80526.
terry.spraker@colostate.edu Next Section Abstract The purpose of our study was
to describe the progressive accumulation of the abnormal conformer of the prion
protein (PrPCWD) and spongiform degeneration in a single section of brain stem
in Rocky Mountain elk (Cervus elaphus nelsoni) with chronic wasting disease
(CWD). A section of obex from 85 CWD-positive elk was scored using the presence
and abundance of PrPCWD immunoreactivity and spongiform degeneration in 10
nuclear regions and the presence and abundance of PrPCWD in 10 axonal tracts,
the subependymal area of the fourth ventricle, and the thin subpial astrocytic
layer (glial limitans). Data was placed in a formula to generate an overall obex
score. Data suggests that PrPCWD immunoreactivity and spongiform degeneration
has a unique and relatively consistent pattern of progression throughout a
section of obex. This scoring technique utilizing a single section of obex may
prove useful in future work for estimating the presence and abundance of PrPCWD
in peripheral tissues and the nervous system in elk with CWD.
Chronic wasting disease elk, obex prion protein spongiform encephalopathy.
ATYPICAL LESION DISTRIBUTION (RBSE 92/21367)
A 6 year old, home bred (HB), Friesian x Holstein cow in a dairy herd in
Aberdeenshirer submitted as a suspect BSE case in the negative study (SE0203),
has been diagnosed as BSE negative on standard, statutory (obex only),
diagnostic criteria at CVL.
Further examination by Dr Jeffrey at Lasswade, as required by the project
design, has revealed vacuolar change in the septal nucleus and putamen which
co-localised with PrP immunoreactivity. No significant lesions were found in any
other part of the brain, neither was PrP found in the medulla.
It is important to note that examination of four brain blocks used earlier
in the epidemic would not have detected the lesion but a 16 block study (as used
in the very days of BSE) would.
FURTHER INFORMATION
The herd of origin has had 15, HB, suspect cases of BSE since July 1989 and
a further case is still alive.
2. Of the 15, eight have been confirmed by standard histopathology and
seven diagnosed negative (including the above case).
3. Fixed brain tissue from the negative cases exists at Lasswade (because
they always collect whole brain in Scotland) but has not so far been examined
further. No frozen tissue was collected so neither SAF nor PrP detection (by
immunoblotting) has been attempted.
4. Mr Wells agrees with Dr Jeffrey's and Dr Simmons' findings.
FURTHER ACTION IN PROGRESS
1. The brain tissue from the negative cases will be examined in detail by
conventional histopathology and ICC.
2. Kevin Taylor and his veterinary colleagues have been alerted to the
situation.
OTHER RECOMMENDED ACTIONS
1. TRANSMISSION Attempt transmission from the 'case' to standard mice
strains. (Note: In regard to strain typing, formalin may have modified strain
phenotype - we need to discuss with NPU). Further transmission studies (eg in
cattle) might be suggested if primary transmission in mice fails. These
proposals have funding implications.
CODE 18-77
93/2.17/1.1
2. PrP GENOTYPING - Although only fixed brain tissue is available we are
considering genotyping from parents/offspring/fixed brain. As a first step we
are attempting to extract DNA from the fixed brain and to amplify the PrP gene
by PCR.
3. John Wilesmith has interrogated the data base for the herd history.
Other than the high proportion of negative cases nothing significant is
apparent.
4. Familial relationships between suspect (including positive and negative)
cases in this herd could be examined and tracings of breeding animals
initiated.
5. Consideration might be given to collecting frozen spinal cord from new
cases in this herd or in dispersals from it for (SAF/PrP examination).
CONCLUSIONS
1. At present it is unclear whether or not this is a singleton incident or
whether the other negative cases in this herd show a similar lesion.
2. The discovery might indicate the existence of a different strain of BSE
from that present in the general epidemic or an unusual response by an
individual host.
3. If further atypical lesion distribution cases are revealed in this herd
then implications of misdiagnosis of 'negative' cases in other herds may not be
insignificant.
4. If this is a new strain all the implications need to be considered
including whether or not to proceed with the further investigation of future
cases negative for BSE on obex examination alone and from which whole brains are
available (as in Scotland) or collected in the future. Also perhaps
investigation of the tissue distribution of infectivity in these animals might
be considered.
5. Animal and public health controls in place should be sufficient since
all tissues (other than brain for diagnosis) are incinerated.
We observe that Dr Tyrrell would wish to be informed of this at an early
opportunity and that the SEAC would wish to discuss it at their meeting in
April.
R BRADLEY
M DAWSON
17 February 1993
CVO - for information and comment on further action please
cc Mr K C Taylor
Dr B J Shreeve
93/2.17/1.2
This minute is re-issued with a wider distribution.
The information contained herein should not be disseminated further except
on the basis of "NEED TO KNOW".
Mr Scudamore
Mr R C Lowson
Dr D Matthews
Mr I Robertson
Dr K MacOwan
Mr C Randall
Mr J W Wilesmith
Mr G A H Wells
Dr M Jeffrey
Dr M Simmons
93/2.17/1.3
IN CONFIDENCE
BSE - ATYPICAL LESION DISTRIBUTION (RBSE 92-21367)
1992
NEW BRAIN DISORDER
3. WHAT ABOUT REPORTS OF NEW FORM OF BSE ?
THE VETERINARY RECORD HAS PUBLISHED AN ARTICLE ON A NEW BRAIN DISORDER OF
CATTLE DISCOVERED THROUGH OUR CONTROL MEASURES FOR BSE. ALTHOUGH IT PRESENTS
SIMILAR CLINICAL SIGNS TO BSE THERE ARE MAJOR DIFFERENCES IN HISTOPATHOLOGY AND
INCUBATION PERIODS BETWEEN THE TWO. MUST EMPHASISE THAT THIS IS _NOT_ BSE.
4. IS THIS NEW BRAIN DISORDER A THREAT ?
WE DO NOT EVEN KNOW WHETHER THE AGENT OF THIS DISEASE IS TRANSMISSIBLE. IN
ANY CASE, CASES SO FAR IDENTIFIED HAD SHOWN SIMILAR SYMPTOMS TO THOSE OF BSE,
AND THEREFORE HAVE BEEN SLAUGHTERED AND INCINERATED, SO THAT IF A TRANSMISSIBLE
AGENT WERE INVOLVED IT WOULD HAVE BEEN ELIMINATED. ...
PLEASE NOTE *
Over the next 8-10 weeks, approximately 40% of all the adult mink on the
farm died from TME.
snip...
The rancher was a ''dead stock'' feeder using mostly (>95%) downer or
dead dairy cattle...
AND THE USDA ET AL KNEW IT TOO ;
"These 9,200 cases were different because brain tissue samples were
preserved with formalin, which makes them suitable for only one type of
test--immunohistochemistry, or IHC."
THIS WAS DONE FOR A REASON!
THE IHC test has been proven to be the LEAST LIKELY to detect BSE/TSE in
the bovine, and these were probably from the most high risk cattle pool, the
ones the USDA et al, SHOULD have been testing. ...TSS
USDA 2003
We have to be careful that we don't get so set in the way we do things that
we forget to look for different emerging variations of disease. We've gotten
away from collecting the whole brain in our systems. We're using the brain stem
and we're looking in only one area. In Norway, they were doing a project and
looking at cases of Scrapie, and they found this where they did not find lesions
or PRP in the area of the obex. They found it in the cerebellum and the
cerebrum. It's a good lesson for us. Ames had to go back and change the
procedure for looking at Scrapie samples. In the USDA, we had routinely looked
at all the sections of the brain, and then we got away from it. They've recently
gone back. Dr. Keller: Tissues are routinely tested, based on which tissue
provides an 'official' test result as recognized by APHIS.
Dr. Detwiler: That's on the slaughter. But on the clinical cases, aren't
they still asking for the brain? But even on the slaughter, they're looking only
at the brainstem. We may be missing certain things if we confine ourselves to
one area.
snip.............
Dr. Detwiler: It seems a good idea, but I'm not aware of it. Another
important thing to get across to the public is that the negatives do not
guarantee absence of infectivity. The animal could be early in the disease and
the incubation period. Even sample collection is so important. If you're not
collecting the right area of the brain in sheep, or if collecting
lymphoreticular tissue, and you don't get a good biopsy, you could miss the area
with the PRP in it and come up with a negative test. There's a new, unusual form
of Scrapie that's been detected in Norway. We have to be careful that we don't
get so set in the way we do things that we forget to look for different emerging
variations of disease. We've gotten away from collecting the whole brain in our
systems. We're using the brain stem and we're looking in only one area. In
Norway, they were doing a project and looking at cases of Scrapie, and they
found this where they did not find lesions or PRP in the area of the obex. They
found it in the cerebellum and the cerebrum. It's a good lesson for us. Ames had
to go back and change the procedure for looking at Scrapie samples. In the USDA,
we had routinely looked at all the sections of the brain, and then we got away
from it. They've recently gone back.
Dr. Keller: Tissues are routinely tested, based on which tissue provides an
'official' test result as recognized by APHIS .
Dr. Detwiler: That's on the slaughter. But on the clinical cases, aren't
they still asking for the brain? But even on the slaughter, they're looking only
at the brainstem. We may be missing certain things if we confine ourselves to
one area.
snip...
FULL TEXT;
Completely Edited Version PRION ROUNDTABLE
Accomplished this day, Wednesday, December 11, 2003, Denver, Colorado
END...TSS
==========
Subject: USDA OIG SEMIANNUAL REPORT TO CONGRESS FY 2007 1st Half (bogus BSE
sampling FROM HEALTHY USDA CATTLE)
Date: June 21, 2007 at 2:49 pm PST
Owner and Corporation Plead Guilty to Defrauding Bovine Spongiform
Encephalopathy (BSE) Surveillance Program
An Arizona meat processing company and its owner pled guilty in February
2007 to charges of theft of Government funds, mail fraud, and wire fraud. The
owner and his company defrauded the BSE Surveillance Program when they falsified
BSE Surveillance Data Collection Forms and then submitted payment requests to
USDA for the services. In addition to the targeted sample population (those
cattle that were more than 30 months old or had other risk factors for BSE), the
owner submitted to USDA, or caused to be submitted, BSE obex (brain stem)
samples from healthy USDA-inspected cattle. As a result, the owner fraudulently
received approximately $390,000. Sentencing is scheduled for May 2007.
snip...
Topics that will be covered in ongoing or planned reviews under Goal 1
include:
soundness of BSE maintenance sampling (APHIS),
implementation of Performance-Based Inspection System enhancements for
specified risk material (SRM) violations and improved inspection controls over
SRMs (FSIS and APHIS),
snip...
The findings and recommendations from these efforts will be covered in
future semiannual reports as the relevant audits and investigations are
completed.
4 USDA OIG SEMIANNUAL REPORT TO CONGRESS FY 2007 1st Half
Wednesday, July 15, 2015
Additional BSE TSE prion testing detects pathologic lesion in unusual brain
location and PrPsc by PMCA only, how many cases have we missed?
***however in 1 C-type challenged animal, Prion 2015 Poster Abstracts S67
PrPsc was not detected using rapid tests for BSE.
***Subsequent testing resulted in the detection of pathologic lesion in
unusual brain location and PrPsc detection by PMCA only.
IBNC Tauopathy or TSE Prion disease, it appears, no one is sure
Posted by flounder on 03 Jul 2015 at 16:53 GMT
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...
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
======================================
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
Monday, March 8, 2010
Canine Spongiform Encephalopathy aka MAD DOG DISEASE
Wednesday, July 29, 2015
Porcine Prion Protein Amyloid or mad pig disease PSE
Friday, January 30, 2015
*** Scrapie: a particularly persistent pathogen ***
P.105: RT-QuIC models trans-species prion transmission
Kristen Davenport, Davin Henderson, Candace Mathiason, and Edward Hoover
Prion Research Center; Colorado State University; Fort Collins, CO USA
The propensity for trans-species prion transmission is related to the
structural characteristics of the enciphering and heterologous PrP, but the
exact mechanism remains mostly mysterious. Studies of the effects of primary or
tertiary prion protein structures on trans-species prion transmission have
relied primarily upon animal bioassays, making the influence of prion protein
structure vs. host co-factors (e.g. cellular constituents, trafficking, and
innate immune interactions) difficult to dissect. As an alternative strategy, we
used real-time quakinginduced conversion (RT-QuIC) to investigate trans-species
prion conversion.
To assess trans-species conversion in the RT-QuIC system, we compared
chronic wasting disease (CWD) and bovine spongiform encephalopathy (BSE) prions,
as well as feline CWD (fCWD) and feline spongiform encephalopathy (FSE). Each
prion was seeded into each host recombinant PrP (full-length rPrP of
white-tailed deer, bovine or feline). We demonstrated that fCWD is a more
efficient seed for feline rPrP than for white-tailed deer rPrP, which suggests
adaptation to the new host.
Conversely, FSE maintained sufficient BSE characteristics to more
efficiently convert bovine rPrP than feline rPrP. Additionally, human rPrP was
competent for conversion by CWD and fCWD. ***This insinuates that, at the level
of protein:protein interactions, the barrier preventing transmission of CWD to
humans is less robust than previously estimated.
================
***This insinuates that, at the level of protein:protein interactions, the
barrier preventing transmission of CWD to humans is less robust than previously
estimated.***
================
*** We hypothesize that both BSE prions and CWD prions passaged through
felines will seed human recPrP more efficiently than BSE or CWD from the
original hosts, evidence that the new host will dampen the species barrier
between humans and BSE or CWD. The new host effect is particularly relevant as
we investigate potential means of trans-species transmission of prion disease.
Monday, August 8, 2011
*** Susceptibility of Domestic Cats to CWD Infection ***
Oral.29: Susceptibility of Domestic Cats to CWD Infection
Amy Nalls, Nicholas J. Haley, Jeanette Hayes-Klug, Kelly Anderson, Davis M.
Seelig, Dan S. Bucy, Susan L. Kraft, Edward A. Hoover and Candace K.
Mathiason†
Colorado State University; Fort Collins, CO USA†Presenting author; Email:
ckm@lamar.colostate.edu
Domestic and non-domestic cats have been shown to be susceptible to one
prion disease, feline spongiform encephalopathy (FSE), thought to be transmitted
through consumption of bovine spongiform encephalopathy (BSE) contaminated meat.
Because domestic and free ranging felids scavenge cervid carcasses, including
those in CWD affected areas, we evaluated the susceptibility of domestic cats to
CWD infection experimentally. Groups of n = 5 cats each were inoculated either
intracerebrally (IC) or orally (PO) with CWD deer brain homogenate. Between
40–43 months following IC inoculation, two cats developed mild but progressive
symptoms including weight loss, anorexia, polydipsia, patterned motor behaviors
and ataxia—ultimately mandating euthanasia. Magnetic resonance imaging (MRI) on
the brain of one of these animals (vs. two age-matched controls) performed just
before euthanasia revealed increased ventricular system volume, more prominent
sulci, and T2 hyperintensity deep in the white matter of the frontal hemisphere
and in cortical grey distributed through the brain, likely representing
inflammation or gliosis. PrPRES and widely distributed peri-neuronal vacuoles
were demonstrated in the brains of both animals by immunodetection assays. No
clinical signs of TSE have been detected in the remaining primary passage cats
after 80 months pi. Feline-adapted CWD was sub-passaged into groups (n=4 or 5)
of cats by IC, PO, and IP/SQ routes. Currently, at 22 months pi, all five IC
inoculated cats are demonstrating abnormal behavior including increasing
aggressiveness, pacing, and hyper responsiveness.
*** Two of these cats have developed rear limb ataxia. Although the limited
data from this ongoing study must be considered preliminary, they raise the
potential for cervid-to-feline transmission in nature.
AD.63:
Susceptibility of domestic cats to chronic wasting disease
Amy V.Nalls,1 Candace Mathiason,1 Davis Seelig,2 Susan Kraft,1 Kevin
Carnes,1 Kelly Anderson,1 Jeanette Hayes-Klug1 and Edward A. Hoover1 1Colorado
State University; Fort Collins, CO USA; 2University of Minnesota; Saint Paul, MN
USA
Domestic and nondomestic cats have been shown to be susceptible to feline
spongiform encephalopathy (FSE), almost certainly caused by consumption of
bovine spongiform encephalopathy (BSE)-contaminated meat. Because domestic and
free-ranging nondomestic felids scavenge cervid carcasses, including those in
areas affected by chronic wasting disease (CWD), we evaluated the susceptibility
of the domestic cat (Felis catus) to CWD infection experimentally. Cohorts of 5
cats each were inoculated either intracerebrally (IC) or orally (PO) with
CWD-infected deer brain. At 40 and 42 mo post-inoculation, two IC-inoculated
cats developed signs consistent with prion disease, including a stilted gait,
weight loss, anorexia, polydipsia, patterned motor behaviors, head and tail
tremors, and ataxia, and progressed to terminal disease within 5 mo. Brains from
these two cats were pooled and inoculated into cohorts of cats by IC, PO, and
intraperitoneal and subcutaneous (IP/SC) routes. Upon subpassage, feline-adapted
CWD (FelCWD) was transmitted to all IC-inoculated cats with a decreased
incubation period of 23 to 27 mo. FelCWD was detected in the brains of all the
symptomatic cats by western blotting and immunohistochemistry and abnormalities
were seen in magnetic resonance imaging, including multifocal T2 fluid
attenuated inversion recovery (FLAIR) signal hyper-intensities, ventricular size
increases, prominent sulci, and white matter tract cavitation. Currently, 3 of 4
IP/SQ and 2 of 4 PO inoculared cats have developed abnormal behavior patterns
consistent with the early stage of feline CWD.
*** These results demonstrate that CWD can be transmitted and adapted to
the domestic cat, thus raising the issue of potential cervid-to- feline
transmission in nature.
www.landesbioscience.com
PO-081: Chronic wasting disease in the cat— Similarities to feline
spongiform encephalopathy (FSE)
FELINE SPONGIFORM ENCEPHALOPATHY FSE
Saturday, January 31, 2015
European red deer (Cervus elaphus elaphus) are susceptible to Bovine
Spongiform Encephalopathy BSE by Oral Alimentary route
*** Singeltary reply ;
ruminant feed ban for cervids in the United States ?
31 Jan 2015 at 20:14 GMT
Terry S. Singeltary Sr.
posted by Terry S. Singeltary Sr. at
3:40 PM
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