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From: TSS ()
Subject: Are cheetahs on the run from prion-like amyloidosis?
Date: May 17, 2008 at 11:49 am PST

Are cheetahs on the run from prion-like amyloidosis?

Byron Caughey* and Gerald S. Baron* Laboratory of Persistent Viral Diseases,
Rocky Mountain Laboratories, National Institute of Allergy and Infectious
Diseases, Hamilton, MT 598940

The misfolding and aggregation of proteins is often an accident waiting to
happen. Consequently, organisms have developed sophisticated chaperone and
quality-control systems to limit abnormal protein interactions and the
accumulation of toxic aggregates (1). However, sometimes these systems can
be overwhelmed, and diseases, namely protein misfolding diseases, can
result. One such disease, amyloid protein A (AA) amyloidosis, is wreaking
havoc in the captive cheetah population, complicating efforts to rescue this
endangered species from extinction (2, 3). One key to managing this fatal
disease in cheetahs is to understand why it is so prevalent. Most cases of
AA amyloidosis in mammals appear to occur spontaneously, usually as a result
of chronic inflammation or genetic peculiarities that predispose the
organism to the deposition of serum amyloid A (SAA) protein in fibrillar
deposits called amyloid (Fig. 1). In this issue of PNAS, Zhang et al. (4)
report that AA amyloid is excreted in the feces of cheetahs with AA
amyloidosis and that this fecal amyloid can in turn promote a similar
disease in mice. These results suggest that cheetah AA amyloidosis may not
be simply a spontaneous disease, but also a natural prion-like,
transmissible protein misfolding disease. Prions are protein-based
infectious agents or elements of inheritance that, unlike conventional
pathogens, lack agent-specific nucleic acid genomes (5, 6). Prions have been
described in both mammals (e.g., bovine spongiform encephalopathy and
Creutzfeldt–Jakob disease) and fungi ([URE3], [PSI], and [Het-s]).
Replication of prions requires a self-propagating modification of an
otherwise non-prion host protein. Usually the mechanism involves the
recruitment of the normal form of the protein into a growing amyloid-like
prion aggregate. In many cases the presence of prions is a disease state,
but some prions play normal physiological roles (7). Although amyloid-like
protein aggregation is typical of many important protein misfolding
diseases, including Alzheimer’s disease and type 2 diabetes, most of these
diseases are not known to be naturally transmissible or heritable because of
transfer of the amyloid. However, experimental inoculations of amyloid
preparations can enhance amyloidosis in nai¨ve mice that are strongly primed
for the development of amyloidosis (8, 9). This suggests that there is
potential for amyloidoses, in general, and AA amyloidosis specifically, to
be transmissible and, hence, prion-like. For such transmissions to be
significant in the real world, there must be practical routes of
transmission and the potential for inducing disease in natural, rather than
artificially primed, hosts. The shedding of AA amyloid into the feces of
cheetahs suggests a potential route of transmission (Fig. 1) (4). Although
the fecal amyloid can promote amyloidosis on i.v. inoculation into mice,
this is only true in mice that were primed for amyloidosis by injections of
an inflammatory chemical (silver nitrate) that dramatically boosts serum SAA
levels. The silver nitrate treatment alone causes spontaneous amyloidosis in
these mice, albeit at a slower pace than when the mice are inoculated with
exogenous amyloid. Thus, it remains to be determined whether fecal amyloid
can actually initiate, rather than enhance, amyloidosis in either mice or
cheetahs and, if so, by what route of inoculation. One possible mode of
entry would be oral because AA amyloid can be active in primed mice when
administered orally as well as intravenously (9, 10). Another potential
route would be direct inoculation of fecal amyloid into the blood stream
through cuts or abrasions. It should be noted that Zhang et al. (4)
inoculated mice with highly concentrated preparations of fecal amyloid.
Hence, it is unknown whether amyloid concentrations in feces would allow tra
nsmission to nai¨ve recipients by any peripheral route. If fecal amyloid can
be transmitted to other captive cheetahs, what makes these animals so
susceptible to AA amyloidosis? The fact that mice can be primed for AA
amyloidosis by inflamm tory stimuli raises the possibility that inflammation
is also important in cheetahs. Indeed, inflammatory diseases are prominent
in captive cheetahs with AA amyloidosis, and a number of precipitating
factors, including chronic infections, diet, and stress, have been
identified (2, 3). Other possibilities include genetic predispositions of
cheetahs to AA amyloidosis because of their SAA sequence or expression
level. Interestingly, a gene polymorphism has been identified in captive
cheetahs that flanks the SAA1 gene and strongly affects its transcriptional
induction in response to inflammation (11). Expression of other proteins can
also profoundly enhance susceptibility of animals to AA amyloidosis, as
shown by modulation of pentraxin levels in hamsters (12). The genetic
homogeneity of captive cheetahs may enhance these susceptibility problems
(11, 13), but does not appear to be the sole issue (3). The very factors
that might make cheetahs susceptible to exogenous AA amyloid ‘‘infections’’
should also potentiate spontaneous AA amyloidosis in these animals. There is
precedent for this in the spontaneous amyloidosis that occurs in silver
nitrate-primed mice. By analogy, it remains possible that the high incidence
of AA amyloidosis in cheetahs is caused by spontaneous disease exacerbated
by the inflammatory stimuli, stresses, and inbreeding of captivity rather
than exposure to fecal amyloid. Further studies will be required to resolve
these questions. AA amyloidosis susceptibility issues may have serious
implications for cheetah conservation efforts. If the objective is to rescue
the wild cheetah population by releasing cheetahs bred in captivity, then it
will be important to know the impact of releasing amyloidotic animals into
the wild. Will AA amyloidosis continue to progress and affect the survival
of released cheetahs? Can the disease be spread to wild cheetahs? One
encouraging observation is that, relative to captive cheetahs, wild Namibian
cheetahs are remarkably free of disease, including inflammatory diseases
such as AA amyloidosis and gastritis (3). Perhaps lower chronic levels of
inflammation, and hence serum SAA levels, make them less susceptible than
captive cheetahs to AA amyloid shed by other animals. Although major
questions remain about the etiology of AA amyloidosis in captive cheetahs,
it may be wise to take measures to limit exposure of cheetahs to potential
sources of amyloid ‘‘infectivity.’’ The demonstration that cheetah AA
amyloid is active in mice indicates that there is cross-species promiscuity
in its amyloid-inducing capacity. This promiscuity might also work in
reverse, rendering cheetahs susceptible to AAamyloid- laden tissues of other
species that might be fed to them. Interestingly, foie gras was recently
shown to contain AA amyloid that could accelerate amyloidosis when fed to
mice (9). Thus, consideration of a variety of potential sources of exposure
for cheetahs seems warranted. Furthermore, if chronic inflammation enhances
disease susceptibility, then anti-inflammatory therapies may be helpful. Is
AA amyloidosis in cheetahs a prion disease? The answer depends on whether AA
amyloidosis in captive cheetahs is caused by spontaneous disease or
transmission of amyloid between animals. Environmental influences on AA
amyloidosis epidemiology could be due to the presence of either ‘‘infectious
’’ amyloid, a prion-like etiology, or to factors that enhance the incidence
of spontaneous disease, i.e., a non-prion etiology. Even if transfer of AA
amyloid between cheetahs enhances AA amyloidosis, the question would remain
as to whether the transferred amyloid initiates the disease de novo or
merely accelerates ongoing disease. The latter scenario would place AA
amyloidosis into a gray area with respect to the basic prion concept. In
this instance, prion transmission would affect the kinetics of the disease
without actually initiating it. Regardless of prion semantics, there could
be practical consequences of such kinetic phenomena in both animals and
humans. For instance, recent studies have shown that in ection of -amyloid
can enhance Alzheimer’s-like amyloidosis in transgenic mice (14). This
raises the possibility that inadvertent transfer of -amyloid from one
person to another could accelerate the neurodegenerative process to the
point where it becomes Alzheimer’s disease as opposed to normal aging. In
this example, as well as in cheetah AA amyloidosis and many other protein
misfolding diseases, the basic problem is likely the outpacing of an
organism’s protein quality control mechanisms. This may sometimes be more a
problem of the rate, rather than of the instigation, of protein misfolding.

Fig. 1. Diagram of AA amyloid formation and the potential prion-like
transmission of AA amyloidosis by fecal shedding and oral uptake of the
amyloid. The photo shows an example of Congo red-stained AA amyloid fibril
deposits in hamster liver tissue (courtesy of John Coe, Rocky Mountain
Laboratories, National Institute of Allergy and Infectious Diseases).

ACKNOWLEDGMENTS. This work was supported by the intramural program of the
National Institute of Allergy and Infectious Diseases, National Institutes
of Health. 1. Balch WE. Morimoto RI, Dillin A, KellyJW(2008) Adapting
proteostasis for disease intervention. Science 319:916–919. 2. Papendick RE,
Munson L, O’Brien TD, Johnson KH (1997) Systemic AA amyloidosis in captive
cheetahs (Acinonyx jubatus). Vet Pathol 34:549–556. 3. MunsonL, et al.
(2005) Extrinsic factors significantly affect patterns of disease in
free-ranging and captive cheetah (Acinonyx jubatus) populations. J Wildl Dis
41:542–548. 4. Zhang B, et al. (2008) Fecal transmission of AA amyloidosis
in the cheetah contributes to high incidence of disease. Proc Natl Acad Sci
USA 105:7263–7268. 5. Prusiner SB (1998) Prions. Proc Natl Acad Sci USA
95:13363–13383. 6. Wickner RB, et al. (2004) Prion genetics: New rules for a
new kind of gene. Annu Rev Genet 38:681–707. 7. Coustou V, Deleu C, Saupe S,
Begueret J (1997) The protein product of the het-s heterokaryon
incompatibility gene of the fungus Podospora anserina behaves as a prion
analog. Proc Natl Acad Sci USA 94:9773–9778. 8. Kisilevsky R, Boudreau L
(1983) Kinetics of amyloid deposition. I. The effects of amyloid-enhancing
factor and splenectomy. Lab Invest 48:53–59. 9. Solomon A, et al. (2007)
Amyloidogenic potential of foie gras. Proc Natl Acad Sci USA
104:10998–11001. 10. Lundmark K, et al. (2002) Transmissibility of systemic
amyloidosis by a prion-like mechanism. Proc Natl Acad Sci USA 99:6979–6984.
11. Zhang B, et al. (March 28, 2008) Characterization of the cheetah serum
amyloid A1 gene: Critical role and functional polymorphism of a cis-acting
element. J Hered, 10.1093/jhered/esn015. 12. Coe JE, Ross MJ (1990)
Amyloidosis and female protein in the Syrian hamster: Concurrent regulation
by sex hormones. J Exp Med 171:1257–1267. 13. O’Brien SJ, et al. (1985)
Genetic basis for species vulnerability in the cheetah. Science 227:1428 –
1434. 14. Meyer-Luehmann M, et al. (2006) Exogenous induction of cerebral
beta-amyloidogenesis is governed by agent and host. Science 313:1781–1784.
7114  www.pnas.orgcgidoi10.1073pnas.0803438105 Caughey and Baron

http://www.pnas.org/cgi/reprint/0803438105v1?etoc

Monday, May 12, 2008

Fecal transmission of AA amyloidosis in the cheetah contributes to high
incidence of disease

http://betaamyloidcjd.blogspot.com/2008/05/fecal-transmission-of-aa-amyloidosis-in.html

Alzheimer's and CJD

http://betaamyloidcjd.blogspot.com/

Saturday, March 22, 2008

10 Million Baby Boomers to have Alzheimer's in the coming decades 2008
Alzheimer’s disease facts and figures

http://betaamyloidcjd.blogspot.com/2008/03/10-million-baby-boomers-to-have.html

Original Paper

Association between Deposition of Beta-Amyloid and Pathological Prion
Protein in Sporadic Creutzfeldt-Jakob Disease

Laura Debatina, Johannes Strefferb, Markus Geissenc, Jakob Matschkec,
Adriano Aguzzia, Markus Glatzela, c

http://betaamyloidcjd.blogspot.com/2008/03/association-between-deposition-of-beta.html

Sunday, April 27, 2008 re-Association between Deposition of Beta-Amyloid and
Pathological Prion Protein in Sporadic Creutzfeldt-Jakob Disease Greetings,

I thought this most important research by Aguzzi et al 'Association between
Deposition of Beta-Amyloid and Pathological Prion Protein in Sporadic
Creutzfeldt-Jakob Disease' most important, and thought further reading of
this study should be at hand.

http://betaamyloidcjd.blogspot.com/2008/04/re-association-between-deposition-of.html

Saturday, May 17, 2008

Are cheetahs on the run from prion-like amyloidosis?

http://betaamyloidcjd.blogspot.com/2008/05/are-cheetahs-on-run-from-prion-like.html

Draft Factual Account #5

10. On 28 June 1986 Mr Jeffrey examined tissue sections taken from the
brain of a nyala which had been kept at Marwell Zoo.(S Jeffrey para 6;
YB86/7.8/1.1 ) This examination, and subsequent consideration of the
report, are described in the CVL DFA.

51. On 10 June 1987 Mr Bradley sent a BSE update to Dr Watson. It
discussed, amongst other things, the nyala case and subsequent paper, the
work of Mr Wilesmith, the upcoming BCVA meeting and the work of Dr
Kimberlin.(YB 87/6.10/1.1 )

63. On 22 June 1987 Mr Bradley sent a memo to Mr Wells detailing actions
taken to date. It noted that publication has been discussed with the CVO
and halted and that there were now at least 9 suspect herds and a case in a
gemsbok at Marwell.(YB 87/6.22/2.1 )

74. On 1 July 1987, Mr Bradley wrote to Mr Jeffrey to tell him that his
article on spongiform encephalopathy in a nyala was not authorised for
publication, and that while he made comparisons with scrapie, the CVO was
unlikely to give his approval.(YB87/6.29/3.1; YB87/7.1/2.1;
YB87/7.1/3.1-3.10 ) This is further discussed in the CVL DFA.

153. On 11 December 1987, Mr Jeffrey's paper on the nyala was submitted
for publication in the journal Veterinary Pathology. The paper had first
been drafted the paper in autumn 1986. (S 64 Jeffrey para 10) The title of
the paper was changed from 'A scrapie-like disorder in a nyala' to 'A
spongiform encephalopathy in a nyala.' Other references to scrapie were
also amended.( S Jeffrey para 10; S 65 Wells para 55; YB87/11.11/2.1;
YB87/11.17/3.1; YB87/11.23/2.1. )

Spongiform encephalopathy in a nyala (Tragelaphus angasi).

Vet Pathol 1988 Sep;25(5):398-9 Jeffrey M, Wells GA Lasswade Veterinary
Laboratory, Midlothian.

166. In January 1988, Mr Wilesmith was informed of the June 1987 case of SE
in the gemsbok. He discovered from the Winchester VIC that both the >nyala
and the gemsbok had received rations containing MBM and this provided
further support for his hypothesis.( S Wilesmith para. 37)

Draft Factual Account #4

28. On 28 June 1986 Dr Jeffrey examined tissue sections taken from the
brain of a nyala which had been kept at Marwell Zoo. (S Jeffrey para 6;
YB86/7.8/1.1 ) The nyala had shown unusual nervous symptoms two weeks prior
to being put down on welfare grounds. These symptoms included 'weaving with
the head and neck, holding the head on its side and frequent nibbling near
the tailbone.'(YB86/6.23/1.1 ) The sections were originally necropsied by
Mr Geoff Holmes at the Winchester VIC.(YB86/5.29/1.1; YB86/6.18/1.1 ) The
nyala (tragelaphus angasi) is not an antelope but belongs to the same
family (species group) as cattle.

29. Dr Jeffrey observed that the brain showed taxonomic lesions of
spongiform encephalopathy and that the similarity of the lesions to natural
sheep scrapie was striking, and indeed he thought that in comparison to
natural sheep scrapie the lesions were particularly florid.(YB86/7.2/1.1; S
Jeffrey para 9 ) The sites (neuroanatomical location) and cellular location
(grey matter neuropil and neuronal cytoplasmic vacuolation) were
distinctive and characteristic of the TSEs. Dr Jeffrey sent a slide of the
nyala brain to Dr Richard Kimberlin at the NPU in the latter quarter of
1986 who 'vividly recollect[ed] seeing the results down the microscope
because the pathology was so striking'.(YB 98/11.18/1.1 )

30. Following a field visit to Marwell Zoo on 21 July
1986,(YB86/7.24/1.1 ) a report was compiled by Mr Holmes at Winchester VIC
and a scientific paper prepared for publication in a journal.(S Jeffrey
para 10 ) Dr Jeffrey conferred with Mr Wells, his line manager at the CVL,
in the preparation of the paper.(S Jeffrey para 9; S Wells 1st para 55 ) Dr
Jeffrey was not sure of the exact date he submitted the paper to the Animal
Health and Veterinary Group (AHVG) for publication but said it was some
time in Autumn 1986.(S Jeffrey para 10; YB86/11.00/1.1 ) Dr Jeffrey did not
form any conclusions about the origins of the disease in this animal, but
he discussed the case with the CVL Epidemiology Department, and they agreed
to keep a 'watching brief' on the situation.(S Wilesmith para 11)

89. On 17 June 1987 the Annual Report of the CVO for 1986 was published,
having been submitted for publication on 1 June 1987.( M24 Tab 2 at 69 )
The Report described the discovery of a 'Scrapie-like disease in a captive
nyala' and noted that 'Transmissible spongiform encephalopathies have been
reported in man, sheep and goats (scrapie), mule deer and mink.'

91. On 19 June 1987 Mr Bradley sent Dr Watson a BSE Update. Amongst other
things it was noted:(YB 87/6.19/3.1-3.2 )

"The final draft Vet Rec paper has been prepared and submitted for
authority to publish. This has been rejected by CVO whilst scrapie is
mentioned. For this and other reasons the paper is temporarily withdrawn
until further information is available"

92. On 19 June 1987 Dr S.H. Done diagnosed spongiform encephalopathy in a
gemsbok from Marwell Park.(YB87/6.19/3.2; YB876.8/3.1; YB87/6.10/3.1;
YB87/6.25/1.1 ) This was the zoo was from which the SE-infected nyala had
come. While the nyala was from the same species group as cattle, the
gemsbok is an African antelope.

100. On 1 July 1987 Mr Bradley wrote to Dr Jeffrey to tell him that his
article on spongiform encephalopathy in a nyala was not authorised for
publication, and that while he made comparisons with scrapie, the CVO was
unlikely to give his approval.(YB87/7.1/3.2; YB87/6.29/3.1; YB87/7.1/2.1 )
The initial title of the paper was 'Scrapie-like disorder in a nyala'.( S
Jeffrey para 12 ) At the request of Tolworth, the title of the paper was
eventually changed to 'Spongiform encephalopathy in a nyala'.(
YB87/11.00/1.1 ) Because of the original references to the scrapie-like
nature of the disorder the paper was delayed for publication and was not
published until September 1988.( J/VP/25/398 ) Dr Jeffrey told the BSE
Inquiry that he resisted the move to alter his paper because it 'would have
been negligent to try and publish that without a reference to scrapie'.(T25
at 32 )

157. On 17 November 1987 Mr Bradley minuted Dr Jeffrey noting that the
title to his nyala paper was likely to be unacceptable to "senior
management" for "veterinary political reasons". He also recommended that
where comparisons were made with scrapie the emphasis ought to be
altered.(YB 87/11.17/1.1 )

433. On 23 October 1989 Dr Watson told Mr Wells that the CVL were to supply
material from the kudu and nyala to the NPU for transmission to mice. Dr
Watson said this was an important transmission experiment designed to
establish the relationship between the disease in zoo animals and cattle.(S
Watson 1st para 134 ) Mr Bradley provided Dr Watson with a list of tissues
that were to be sent to the NPU on 24 November 1989.(YB89/10.24/4.1 )

================================================

BSE Inquiry site Draft Factual Account 13 extracts related to zoo animals:

19. On 24 January 1990 Mr Bradley sent to Dr Watson a summary of the
main points of a meeting held with the Minister the same day.(20) The minute
noted: "The Minister played Devil's advocate in relation to: ... 5. MBM
exports unethical. All should be labelled & a letter should be sent to all
countries to which MBM was exported should be sent." [No such letter was
sent.]

28. By 12 February 1990 the nyala and kudu tissues and the placenta had been
inoculated into mice at the NPU.(33) After his investigations into the
alimentary tract, ... Mr Bradley said in a minute dated 12 February 1990
that:(36) "It is very clear that it is important to initiate studies now in
a much wider range of tissues and in multiple specimens than can be
accommodated in the annual quota of 30 for the next two years." Mr Bradley
attached a table showing the progress of infectivity studies:..fixed nyala
brain, fixed kudu brain, buffy coat.

57. On 17 September 1990 Mr Bradley circulated a minute with regards to
an offer by Dr Schellekers of the Netherlands to collaborate on attempting
to transmit BSE to chimpanzees.(YB90/9.17/1.1) Mr Wells and Dr Rosalind
Ridley, who was conducting the marmoset experiment, told Mr Bradley that
they did not feel there was any greater justification for an attempted
transmission in chimpanzees than marmosets.(S Bradley 3rd para 40 ) Mr
Bradley passed on this view to the CVO.(YB90/9.23/1.1; YB90/9.26/3.1 ).
[This is ignorant beyond belief.]

67. In Spring 1991 Mr McGill performed a review of 200 brains that had,
using the obex histopathological method, been deemed BSE-negative.(110) This
diagnostic approach, that had been developed for use within the VIS, used a
single section from the medulla to look for spongiform change. In his review
Mr McGill examined other parts of the brain.(111) In his statement to the
BSE Inquiry Mr McGill said:

Upon closer examination, three of the 200 'BSE-negative' brains proved
positive for spongiform changes diagnostic of BSE.(112) This represents an
overall diagnostic accuracy of 99.85%, exceeding the 99.6% previously
published for the same standard diagnostic technique. Despite this, at the
behest of MAFF managers, the emphasis of the study and its provisional title
had to be changed, from accurately representing the whole negative 10%, to a
study examining this 10% minus any mention whatsoever of BSE-affected cattle
going undiagnosed. I therefore had to reluctantly locate and analyse three
new BSE-negative suspect brains.(113)

76. In mid-1991 it was decided that a proposed survey of 300 deer brains
would proceed.(124) As with the hound survey, there were difficulties in
collecting the material in a manner optimal for histopathological
examinations.(See YB92/11.4/2.1) During the period 1986 to 1996, 26 deer
brains were referred for examination to the Consultant Pathology Unit at the
CVL, but none of these showed evidence of an SE.

103. On 16 July 1992 a meeting was held at CVL to discuss the research
proposals relating to the studies on SEs in a greater kudu at a zoo. (S
Bradley 3rd para 65 ) Three main experiments were proposed: to determine the
distribution of agent in tissues; to study the epidemiology; and to strain
type isolates from a brain of a new case of spongiform encephalopathy.
Formal proposals were later drawn up and Mr Bradley became the Project
Officer for the experiments.

108. Mr Bradley and Mr Dawson met staff at London Zoo on 23 March 1993
to discuss tissue selection for the proposed transmission studies on
BSE-infected kudu material.(166) The Zoo did not want to keep the kudu, but
moving them to the CVL was ruled out because of inadequate facilities to
care for them. The investigations into the distribution of the SE agent in
various tissues began in June 1993.

121. On 9 October 1993 Mr Wilesmith and others published a paper on the
additional cases of TSE in the herd of greater kudu at London Zoo.(S
Wilesmith 2nd para 95 ) On the basis of feeding histories, the authors
concluded that horizontal transmission had occurred. However, subsequent
investigations based at the zoo revealed that the affected animals were most
likely to have been infected from the feedborne source.

143. On 3 July 1994 Mr Bradley was informed that two more kudu were to
be culled.( Bradley 3rd para 86 ) He visited the London Zoo on 21 July 1994
to review the progress of the studies on TSEs in zoo animals. Necropsies
were to be carried out on the kudu and tissues collected for further
transmission studies. At this stage the mice that had been inoculated with
kudu tissues in August and September 1993 had not succumbed to spongiform
encephalopathy. The Zoo authorities wanted to move the kudu because of the
possibility of bad publicity.(YB95/2.10/1.6) This was discussed at a SEAC
meeting on 2 February 1995. The meeting agreed that the risk to Zoo visitors
was minuscule or non-existent. Mr Bradley's case control study indicated
that infected feed was the most probable cause of the BAB kudu SE cases.


=-=-=-=-=-=-=-=-

46. On 28 June 1990 Mr Bradley informed Mr Wells that a survey of hounds was
to commence.(68) The hound survey arose because the Tyrrell Committee had
recognised that domestic pets might prove susceptible to the unconventional
agent of BSE and recommended monitoring the health of animals fed offal,
carcases or meat and bone meal.(M11a Tab 8 )

47. A total of 444 hound brains of mixed breeds from 101 kennels across the
United Kingdom were collected and examined. Histopathological changes
consistent with a florid spongiform encephalopathy similar to that reported
in cats was not observed. However, the report of the survey identified
serious flaws in the survey's design. Mr Wells said in a minute to Mr
Bradley in October 1991 that 'the survey as designed has little to offer
scientifically'.(YB91/10.17/1.1)

54. On 20 August 1990 Mr Wells confirmed the parenteral transmission of BSE
to a pig.(YB90/7.20/2.1) The pig was inoculated in February/March of 1989
and was slaughtered in July 1990.(S Wells 2nd para 40) An interim report was
prepared for SEAC(84) and a press conference was held on 24 September 1990
to announce the parenteral transmission of BSE to pigs.(85) The transmission
of BSE to pigs was a major factor in the ban on SBOs being extended to all
animal feed. Experiments were also conducted by orally dosing pigs with BSE
infected material but when the pigs were killed after seven years they were
not found to be incubating the disease.(S Wells 2nd para 40 )

55. By August 1990 a total of 10 cases of FSE in domestic cats had been
confirmed.(S Wilesmith 2nd para 109 ) Mr Wilesmith designed a questionnaire
to be completed by the veterinarians who clinically identified FSE for the
purposes of an epidemiological investigation. In addition to this
investigation, the University of Bristol was subsequently granted a MAFF
contract for a study in collaboration with the NPU to ascertain whether the
condition in cats was transmissible to mice and, if so, to undertake strain
typing of the agent.(S Wells 2nd para 104; YB 92/6.19/5.1 ) Mr Wells was
appointed Project Officer to monitor the study. When the study was completed
it showed that the disease in cats was transmissible and that similarities
in the biological characteristics of FSE and BSE on transmission to mice
indicated that the two diseases probably arose from a common
source.(J/VR/134/449 )


64. In February 1991 Mr Mark Robinson began studies on the transmission of
BSE to mink.(S Wilesmith 2nd paras 117-118 ) This study was done in
collaboration with the United States Department of Agriculture (USDA), the
Agricultural Research Service (ARS), and the Department of Veterinary
Science at the University of Wisconsin, USA. The results of this study were
discussed at the 10th CVL/NPU BSE R&D meeting held on 27 April
1993.(YB93/4.27/1.1) The results indicated that mink were susceptible to
BSE, and in contrast to previous attempts to transmit scrapie to the
species, were susceptible by the oral route of challenge.(J/JVIR /75/2151)

99. On 11 April 1992 Mr Bradley prepared a paper for the Lamming Expert
Committee on Animal Feedingstuffs.(153) Some of the areas covered in the
paper were tallow, the danger of BSE to pigs, the effect of the species
barrier, tissue infectivity of lambs and calves, scrapie incidence and the
danger of dogs developing SEs.

116. In July 1993 studies involving the oral exposure of pigs to scrapie
were started the CVL.(179) Such studies were recommended by the expert
committee on feedingstuffs chaired by Professor Lamming, because it was
found that pigs had been orally exposed not only to BSE but also to scrapie.
The pigs were orally exposed to scrapie-infected brain material in November
1993 and while the experiment remains in progress, no pigs have been shown
to have developed the disease to date.

123. In December 1993 Dr Ken Charlton of the Animal Disease Research
Institute, Nepean, Ontario, Canada, visited the CVL bringing material from a
suspect case of BSE in Canada. The CVL confirmed that the case was a BSE
case and reported it to the Canadian authorities.(189) in 1994.

152. On 13-16 February 1995 ... ...BSE to pigs - Further work to clarify
the finding of non-specific vacuolation in the brains of control pigs was
needed.

...BSE to chickens - Sub-passage in chickens and mice of various tissues
from experimentally infected birds was needed to clarify the findings of
neurological signs without neuropathology in inoculated birds.


==-=-=-=-

bibliography:

Vet Rec 1997 Sep 13;141(11):270-1
Baron-T, Belli-P Madec-J-Y Moutou-F Vitaud-C Savey-M
Spongiform encephalopathy in an imported cheetah in France.
CNEVA-Lyon, Laboratoire de Pathologie Bovine, France.

Proc Soc Exp Biol Med 1996 Apr;211(4):306-22
Narang H
Origin and implications of bovine spongiform encephalopathy. [tiger]

Vet Rec. 1994 Nov 12;135(20):488.
Benbow G.
Spongiform encephalopathies in zoo animals. comment

Vet Rec 1994 Oct 29;135(18):440
Swainston J.
comment

Vet Rec 1994 Sep 24;135(13):296-303
Kirkwood JK, Cunningham AA
Epidemiological observations on spongiform encephalopathies

Vet Rec 1994 Feb 12;134(7):167-8
Kirkwood JK, Cunningham AA, Austin AR, Wells GA, Sainsbury AW
Spongiform encephalopathy in a greater kudu

Vet Rec. 1993 Oct 9;133(15):360-4.
Kirkwood JK, et al.
Spongiform encephalopathy in a herd of greater kudu

Vet Rec. 1993 Jan 16;132(3):68.
Cunningham AA, et al.
Transmissible spongiform encephalopathy in greater kudu


Vet Rec. 1992 Nov 7;131(19):431-4.
Willoughby K, et al.
Spongiform encephalopathy in a captive puma

Aust Vet J 1992 Jul;69(7):171
Peet RL, Curran JM
Spongiform encephalopathy in an imported cheetah

Vet Rec 1992 Apr 25;130(17):365-7
Kirkwood JK, Wells GA, Cunningham AA, Jackson SI, Scott AC, Dawson M,
Wilesmith JW
Scrapie-like encephalopathy in a greater kudu

Acta Neuropathol (Berl) 1992;84(5):559-69
Jeffrey M, Scott JR, Williams A, Fraser H
Ultrastructural features of spongiform encephalopathy

Vet Rec. 1991 Oct 5;129(14):320
Synge BA, et al.
Spongiform encephalopathy in a Scottish cat.

Vet Rec 1991 Sep 14;129(11):233-6
Wyatt JM, Pearson GR,
Naturally occurring scrapie-like s

Vet Rec. 1991 Jun 1;128(22):532.
Pearson GR, et al.
Feline spongiform encephalopathy.

Vet Rec. 1991 Mar 30;128(13):311.
Kock R.
Spongiform encephalopathies in ungulates.

Vet Rec. 1991 Feb 2;128(5):115.
Gibson PH.
Spongiform encephalopathies in ungulates. comment

Vet Rec 1990 Dec 15;127(24):586-8
Leggett MM, Dukes J, Pirie HM
A spongiform encephalopathy in a cat.

Done JT.
Vet Rec. 1990 Nov 10;127(19):484.
Spongiform encephalopathy in pigs.

Vet Rec. 1990 Oct 27;127(17):418-20.
Kirkwood JK, et al.
Spongiform encephalopathy in an arabian oryx (Oryx leucoryx) and a greater
kudu.

Vet Rec. 1990 Sep 29;127(13):338.
Dawson M, et al.
Primary parenteral transmission of bovine spongiform encephalopathy to the
pig.

Vet Rec. 1990 May 19;126(20):513
no authors listed
Spongiform encephalopathy in a cat.

Vet Rec 1990 May 12;126(19):489-90
Gibson PH
Spongiform encephalopathy in an eland.

Nature. 1990 Mar 15;344(6263):183
Aldhous P.
Antelopes die of "mad cow" disease.

Vet Rec 1990 Apr 21;126(16):408-9
Fleetwood AJ, Furley CW
Spongiform encephalopathy in an eland.

Vet Pathol. 1988 Sep;25(5):398-9
Jeffrey M, Wells GA
Spongiform encephalopathy in a nyala (Tragelaphus angasi)
Lasswade Veterinary Laboratory, Midlothian


Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518




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