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CHEETAH AT ZOO IN NUREMBERG CONTRACTS FSE

flounder

Well-known member
Subject: CHEETAH AT ZOO IN NUREMBERG CONTRACTS FELINE SPONGIFORM ENCEPHALOPATHY FSE
Date: September 7, 2007 at 8:26 am PST

New BSE-like disease found in cheetah
06/09/2007 - 17:52:28

A cheetah at a zoo in Nuremberg has died after contracting an illness similar to mad cow disease, becoming the first confirmed case in Germany of feline spongiform encephalopathy (FSE), city authorities said today.

Lulu, a female cheetah born in 1998, had suffered for six weeks from problems that included trouble balancing and weakness in her hind legs, the Nuremberg city government said in a statement.

The animal eventually was put to sleep, and tests by Bavarian and federal labs were positive for FSE, it added.

It was unclear how and when Lulu became infected with the disease, which has a several-year incubation period, but Nuremberg authorities said it likely happened in the Netherlands, where she was born.

Lulu moved to Germany at the age of 15 months, returned to the Netherlands five years later and arrived at the Nuremberg zoo in March 2006.


http://www.breakingnews.ie/world/mhcwgbqlkfcw/


http://www.eveningecho.ie/news/bstory.asp?j=230658672&p=z3x659378&n=230659432


http://www.live-pr.com/en/bse-like-disease-detected-in-german-zoo-s-r1048136284.htm


GREETINGS,

interesting to say the least. how could this cheetah have contracted FSE?

feed with FSE ?

casual contact with FSE in zoo ?

remember the man and his cat whom both had sporadic CJD;


In October 1998 the simultaneous occurrence of spongiform encephalopathy
in a man and his pet cat was reported. The report from Italy noted that
the cat did not display the same clinical features as FSE cases
previously seen. Indeed, the presence of a new type of FSE was
suggested. The man was diagnosed as having sporadic CJD, and neither
case (man nor cat) appeared to be affected by a BSE-related condition.
http://www.defra.gov.uk/animalh/bse/bse-science/level-4-othertses.html:

Image] Research letters Volume 352, Number 9134 [Image] 3 October1998[Previous] [Next] [Image][Image]
Simultaneous occurrence of spongiform encephalopathy in a manand his cat in Italy

[Image] Gianluigi Zanusso, Ettore Nardelli, Anna Rosati, GianMaria Fabrizi, SergioFerrari, Antonella Carteri, Franco De Simone, Nicola Rizzuto, SalvatoreMonaco

Transmissible spongiform encephalopathies (TSE) encompass inherited,acquired, and sporadic mammalian neurological disorders, and arecharacterised by the conversion of the cellular prion protein (PrP) in aninsoluble and protease-resistant isoform (PrPres). In human TSE, four typesof PrPres have been identified according to size and glycoform ratios, whichmay represent different prion strains. Type-1 and type-2 PrPres areassociated with sporadic Creutzfeldt-Jakob disease (CJD), type 3 withiatrogenic CJD, and type 4 with variant CJD.1,2 There is evidence thatvariant CJD is caused by the bovine spongiform encephalopathy (BSE)-prionstrain.2-4 The BSE strain has been identified in three cats with felinespongiform encephalopathy (FSE), a prion disease which appeared in 1990 inthe UK.5 We report the simultaneous occurrence of sporadic CJD in a man anda new variety of FSE in his cat. A 60-year-old man, with no unusual dietary habits, was admitted in November,1993, because of dysarthria, cerebellar ataxic gait, visual agnosia, andmyoclonus. An electroencephalogram (EEG) showed diffuse theta-deltaactivity. A brain magnetic resonance imaging scan was unremarkable. 10 dayslater, he was speechless and able to follow only simple commands. RepeatEEGs showed periodic triphasic complexes. 2 weeks after admission, he wasmute, akinetic, and unable to swallow. He died in early January, 1994. His 7-year-old, neutered, female shorthaired cat presented in November,1993, with episodes of frenzy, twitching of its body, and hyperaesthesia.The cat was usually fed on canned food and slept on its owner's bed. Nobites from the cat were recalled. In the next few days, the cat becameataxic, with hindquarter locomotor dysfunction; the ataxia got worse andthere was diffuse myoclonus. The cat was killed in mid-January, 1994. No pathogenic mutations in the patient's PrP gene were found. The patientand the cat were methionine homozygous at codon 129. Histology of thepatient's brain showed neocortical and cerebellar neuronal loss,astrocytosis, and spongiosis (figure A). PrP immunoreactivity showed apunctate pattern and paralleled spongiform changes (figure B). The cat'sbrain showed mild and focal spongiosis in deeper cortical layers of all fourlobes (figure C), vacuolated cortical neurons (figure D), and mildastrogliosis. The cerebellar cortex and the dentate nucleus were gliosed.Immunoreactive PrP showed a punctate pattern in neocortex, allocortex, andcaudate nucleus (figure E). Western blot analysis of control and affectedhuman and cat brain homogenates showed 3 PrP bands of 27-35 kDa. Afterdigestion with proteinase K and deglycosylation, only samples from theaffected patient and cat showed type-1 PrPres, with PrP glycoform ratioscomparable to those observed in sporadic CJD1 (details available fromauthor). [Image] Microscopic sections of patient and cat brains A: Occipital cortex of the patient showing moderate spongiformdegeneration and neuronal loss (haematoxylin and eosin) and B: punctateperineuronal pattern of PrP immunoreactivity; peroxidaseimmunohistochemistry with monoclonal antibody 3F4. C: cat parietal cortexshowing mild spongiform degeneration (haematoxylin and eosin).D:vacuolated neurons (arrow, haematoxylin and eosin), E: peroxidaseimmunohistochemistry with antibody 3F4 shows punctate perineuronaldeposition of PrP in temporal cortex. This study shows a spatio-temporal association between human and felineprion diseases. The clinical features of the cat were different frompreviously reported cases of FSE which were characterised by gradual onsetof behavioural changes preceding locomotor dysfunction and ataxia.5Neuropathological changes were also at variance with the diffuse spongiosisand vacuolation of brainstem neurons, seen in FSE.5 The synaptic pattern ofPrP deposition, similar in the cat and in the patient, was atypical for aBSE-related condition. Evidence of a new type of FSE was further provided bythe detection of a type-1 PrPres, other than the BSE-associated type 4.2Taken together, our data suggest that the same agent strain of sporadic CJDwas involved in the patient and in his cat. It is unknown whether these TSE occurred as the result of horizontaltransmission in either direction, infection from an unknown common source,or the chance occurrence of two sporadic forms.

1 Parchi P, Castellani R, Capellari S, et al. Molecular basis of phenotypicvariablity in sporadic Creutzfeldt-Jakob disease. Ann Neurol 1996; 39:767-78 [PubMed]. 2 Collinge J, Sidle KCL, Meads J, Ironside J, Hill AF. Molecular analysis ofprion strain variation and the aetiology of 'new variant' CJD. Nature 1996;383: 685-90 [PubMed]. 3 Bruce ME, Will RG, Ironside JW, et al. Transmissions to mice indicate that'new variant' CJD is caused by the BSE agent. Nature 1997; 389: 498-501[PubMed]. 4 Hill AF, Desbruslais M, Joiner S, et al. The same prion strain causes vCJDand BSE. Nature 1997; 389: 448-50 [PubMed]. 5 Pearson GR, Wyatt JM, Henderson JP, Gruffydd-Jones TJ. Feline spongiformencephalopathy: a review. Vet Annual 1993; 33: 1-10.
------------------------------------------------------------------------
Sezione di Neurologie Clinica, Dipartimento di Scienze Neurologiche e dellaVisione, Università di Verona, Policlinico Borgo Roma, 37134 Verona, Italy(S Monaco; e mail [email protected]); and Istituto ZooprofilatticoSperimentale della Lombardia e dell' Emilia, Brescia
=========================================TSS
indeed there have been 4 documented cases of TSE in Lions to date.
Lion 32 December 98 Born November 86
Lion 33 May 1999 (euthanased) Born November 81.
Lion 36 Euthanased August 2000 Born July 87. Deteriorating hind limb
ataxia.
Lion 37 Euthanased November 2001 Male, 14 years. Deteriorating hind
limb ataxia since September 2001. (Litter mate to Ref. 36.)
http://www.defra.gov.uk/animalh/bse/index.html
go to the url above, on the bar at the top, click on _statistics_,
then in middle of next page, click on_other TSEs_.
or go here;
http://www.defra.gov.uk/animalh/bse/bse-statistics/level-3-tsestat.html:

and
http://www.defra.gov.uk/animalh/bse/bse-science/level-4-othertses.html:

http://www.bseinquiry.gov.uk/files/yb/1992/11/13001001.pdf:

also;
Reports on the clinical symptoms presented by these cats give a
relatively homogeneous picture: Affected cats show a lack of
coordination with an ataxia mainly of the hind limbs, they often fall
and miss their target when jumping. Fear and increased aggressiveness
against the owner and also other animals is often seen. They do not
longer tolerate to be touched (stroked) and start hiding. These
behavioural chances might be the result of a hypersensibility to touch
and noise, but also to increased fear. Excessive salivation is another
more frequently seen symptom. Cats with FSE in general show severe
behavioural disturbances, restlessness and depression, and a lack of
coat cleaning. Symptoms in large cats in general are comparable to those
in domestic cats. A
report on FSE (in german) has been presented in 2001 in the Swiss FVO
Magazin. A paper on the first FSE case in a domestic cat in Switzerland
is currently in press in the Journal Schweizer Archiv für Tierheilkunde
(SAT).
http://www.neurocenter-bern.ch/tse_e.shtml:


TSS
 

Kathy

Well-known member
Remeber how the Netherlands fed their farmed mink - reindeer that had levels of Cesium 137 that were too high for "human" consumption... but OKY DOKY for the mink. www.ccnrg.org "Radioactive Legacy 2007 Stockholm, Sweden Conference, Dr. Gordon Edwards"

I suggest examining where the Netherland zoo got their meat for Lulu.... AND the food they feed Lulu's mother... it was very likely contaminated with high levels of Cesium 137. The radiation decay effect won't go away.... Chernobyl fallout, and continued use of nuclear reactors/DU weapons, pollute the environment. Half-life of Cesium 137 is 30.3 years. I'd also be asking how often she, or her mother, were treated with OPs to get rid of bugs.

Recently on Canadian news program, a group looking for "items" from home for the troops in Afganastan suggested Canadians send "flea collars" so the soldiers could wear them around their necks.....

Quote from a web page on depleted uranium and Gulf War Syndrome:

http://planetquo.com/Gulf-War-Syndrome-Depleted-Uranium-And-The-Dangers-Of-Low-Level-Radiation

Caution, some pictures on this site might disturb you. The effects of depleted uranium on the fetus and young children are horrendous.

This quote was from the section entitled: "A Book By Dr. E.B. Burlakova"


"For all of the parameters a bimodal dose-effect dependence was discovered, i.e. the effect increased at low doses, reached its low-dose maximum, and then decreased in some cases, the sign of the effect changed to the opposite - or 'benefit' effect - and increased again as the dose was increased." Dr. Burlakova has speculated that at the lowest experimental doses used in this research, the repair mechanism of the cells was not triggered. It became activated at the point of the low-dose maximum, providing a 'benefit' until it was overwhelmed and the damage began again to increase with dose. This may well be the case.

However, the unexpected effects of low dose/slow-dose rate exposure to ionising radiation can also be attributed to biological mechanisms, other than the direct DNA damage hypothesis usually used by radiation physicists. These secondary mechanisms are specific to the low- dose conditions. Three such secondary mechanism have been observed by scientists: the Petkau effect, monocyte depletion, and deformed red blood cells.

*The Petkau effect: discovered by Abram Petkau at the Atomic Energy of Canada Ltd. Whiteshell Nuclear Research Establishment, Manitoba, Canada in 1972. Dr. Petkau discovered that at 26 rads per minute (fast-dose rate) it required a total dose of 3,500 rads to destroy a cell membrane. However, at 0.001 rad per minute (slow dose rate), it required only 0.7 rad to destroy the cell membrane. The mechanism at the slow-dose rate is the production of free radicals of oxygen (O2 with a negative electrical charge) by the ionising effect of the radiation.

The sparsely distributed free radicals generated at the slow-dose rate have a better probability of reaching and reacting with the cell wall than do the densely crowded free radicals produced by fast-dose rates. These latter recombine quickly. Moreover, the slight electrical charge of the cell membrane attracts the free radicals in the early stages of the reaction (low total dose). Computer calculations have shown that the attraction weakens with greater concentrations of free radicals. The traditional radiation biologist has tested only high-dose reactions, and looked for direct damage to the membrane by the radiation.


I couldn't have said this better, the biological mechanisms to protect the cell from ionizing radiation (SODII - a manganese based antioxidant found in the cell, produced by the mitochondria) increases to fight off the dangerous "reactive oxygen species" (ROS) created by the low level radionuclide's presence in the cell. This defense mechanism can put up a good fight so long as the radiation exposure eventually ends. In the case of TSEs, the exposure just keeps happening and the defense mechanism is OVERWHELMED, especially when a mineral imbalance and copper deficiency accompany. It is only at this point that symptoms of the disease become apparent. This is what some call an incubation period.

It takes time for these internalized radionuclides to OVERWHELM the antioxidants and protective mechanisms of the cell and body. Other mechanisms, like "stem cells" which are capable of replacing the lost cells must be sent from the bone marrow. These are also OVERWHELMED and their capacity to function slowly destroyed. So many of the radionuclides accumulate in the bones. (Cesium 137 accumulates in muscle).

READ MORE at the link.....
 

flounder

Well-known member
lots of previous fse cheetas

the new one could simply be an export from the UK that is making the rounds, like the others. for sure the netherlands knows the exact history as all zoos maintain precise records on rare species.

the UK fed split skulls of cattle to their large zoo cats ... duh

http://www.mad-cow.org/zoo_cites_annotated.html

The 82 zoo animals with BSE as of 22 April 1999.:

Id TSE Genus Species Subsp Birth Origin Death Place of Death
1 + Actinonyx jubatus cheetah 1986 Marwell zoo 1991 Pearle Coast AU
Duke + Actinonyx jubatus cheetah 1984 Marwell zoo 1992 Colchester zoo? UK
Saki + Actinonyx jubatus cheetah 1986 Marwell zoo 1993 unknown UK
Mich + Actinonyx jubatus cheetah 1986 Whipsnade 1993 Whipsnade UK
Fr1 + Actinonyx jubatus cheetah 1987 Whipsnade 1997 Safari de Peaugres FR
Fr2 + Actinonyx jubatus cheetah 1991 Marwell zoo 1997 Safari de Peaugres Fr
xx + Actinonyx jubatus cheetah 19xx xxx zoo 199x Fota zoo IR
yy + Actinonyx jubatus cheetah 19xx yyy zoo 1996+ yyyy zoo UK
zz + Actinonyx jubatus cheetah 19xx zzz zoo 1996+ yyyy zoo UK

aaa + Felis concolor puma 1986 Chester zoo 1991 Chester zoo UK
yy + Felis concolor puma 1980 yyy zoo 1995 yyyy zoo UK
zz + Felis concolor puma 1978 zzz zoo 1995 zzzz zoo UK

xxx + Felis pardalis ocelot 1987 xxx 1994 Chester zoo UK
zzz + Felis pardalis ocelot 1980 zzz 1995 zzzz zoo UK

85 + Felis catus cat 1990+ various 1999+ various UK LI NO
19 + Canis familia. dog 1992+ various 1999+ various UK

Fota + Panthera tigris tiger 1981 xxx zoo 1995 xxxx zoo UK
yy + Panthera tigris tiger 1983 yyy zoo 1998 yyyy zoo UK

Lump + Panthera leo lion 1986 Woburn SP 1998 Edinburgh zoo UK [since 1994]


or see the links under Zoo BSE at http://www.mad-cow.org/00/sci_archive_frame.html

Zoo Prion Disease: review of scientific literature
Database of 82 zoo animals with prion disease
Switcheroo -- mysteries at the MAFF home page
More cheetah TSE 9 years after 'ban'
The case of the missing pumas, tigers, ocelots, and lion
How many house cats really had TSE?
The Bristol Zoo tigers: 1970-77
Horizontal transmission demonstrated in kudu
Eland, nyala, bison, ankole, arabianory, and scimitar-horned oryx
French primate disaster
Primate BSE quarantine recommendations
TSEs in primates: brief literature survey
Lemur prion sequences predicted
Prosimians: which animals are involved so far?
Earlier BSE problems at French, Australian, and Irish zoos
Further blow aimed at surviving primates
Which zoos, which primates, how many animals?


tss


flounder said:
Subject: CHEETAH AT ZOO IN NUREMBERG CONTRACTS FELINE SPONGIFORM ENCEPHALOPATHY FSE
Date: September 7, 2007 at 8:26 am PST

New BSE-like disease found in cheetah
06/09/2007 - 17:52:28

A cheetah at a zoo in Nuremberg has died after contracting an illness similar to mad cow disease, becoming the first confirmed case in Germany of feline spongiform encephalopathy (FSE), city authorities said today.

Lulu, a female cheetah born in 1998, had suffered for six weeks from problems that included trouble balancing and weakness in her hind legs, the Nuremberg city government said in a statement.

The animal eventually was put to sleep, and tests by Bavarian and federal labs were positive for FSE, it added.

It was unclear how and when Lulu became infected with the disease, which has a several-year incubation period, but Nuremberg authorities said it likely happened in the Netherlands, where she was born.

Lulu moved to Germany at the age of 15 months, returned to the Netherlands five years later and arrived at the Nuremberg zoo in March 2006.


http://www.breakingnews.ie/world/mhcwgbqlkfcw/


http://www.eveningecho.ie/news/bstory.asp?j=230658672&p=z3x659378&n=230659432


http://www.live-pr.com/en/bse-like-disease-detected-in-german-zoo-s-r1048136284.htm


GREETINGS,

interesting to say the least. how could this cheetah have contracted FSE?

feed with FSE ?

casual contact with FSE in zoo ?

remember the man and his cat whom both had sporadic CJD;


In October 1998 the simultaneous occurrence of spongiform encephalopathy
in a man and his pet cat was reported. The report from Italy noted that
the cat did not display the same clinical features as FSE cases
previously seen. Indeed, the presence of a new type of FSE was
suggested. The man was diagnosed as having sporadic CJD, and neither
case (man nor cat) appeared to be affected by a BSE-related condition.
http://www.defra.gov.uk/animalh/bse/bse-science/level-4-othertses.html:

Image] Research letters Volume 352, Number 9134 [Image] 3 October1998[Previous] [Next] [Image][Image]
Simultaneous occurrence of spongiform encephalopathy in a manand his cat in Italy

[Image] Gianluigi Zanusso, Ettore Nardelli, Anna Rosati, GianMaria Fabrizi, SergioFerrari, Antonella Carteri, Franco De Simone, Nicola Rizzuto, SalvatoreMonaco

Transmissible spongiform encephalopathies (TSE) encompass inherited,acquired, and sporadic mammalian neurological disorders, and arecharacterised by the conversion of the cellular prion protein (PrP) in aninsoluble and protease-resistant isoform (PrPres). In human TSE, four typesof PrPres have been identified according to size and glycoform ratios, whichmay represent different prion strains. Type-1 and type-2 PrPres areassociated with sporadic Creutzfeldt-Jakob disease (CJD), type 3 withiatrogenic CJD, and type 4 with variant CJD.1,2 There is evidence thatvariant CJD is caused by the bovine spongiform encephalopathy (BSE)-prionstrain.2-4 The BSE strain has been identified in three cats with felinespongiform encephalopathy (FSE), a prion disease which appeared in 1990 inthe UK.5 We report the simultaneous occurrence of sporadic CJD in a man anda new variety of FSE in his cat. A 60-year-old man, with no unusual dietary habits, was admitted in November,1993, because of dysarthria, cerebellar ataxic gait, visual agnosia, andmyoclonus. An electroencephalogram (EEG) showed diffuse theta-deltaactivity. A brain magnetic resonance imaging scan was unremarkable. 10 dayslater, he was speechless and able to follow only simple commands. RepeatEEGs showed periodic triphasic complexes. 2 weeks after admission, he wasmute, akinetic, and unable to swallow. He died in early January, 1994. His 7-year-old, neutered, female shorthaired cat presented in November,1993, with episodes of frenzy, twitching of its body, and hyperaesthesia.The cat was usually fed on canned food and slept on its owner's bed. Nobites from the cat were recalled. In the next few days, the cat becameataxic, with hindquarter locomotor dysfunction; the ataxia got worse andthere was diffuse myoclonus. The cat was killed in mid-January, 1994. No pathogenic mutations in the patient's PrP gene were found. The patientand the cat were methionine homozygous at codon 129. Histology of thepatient's brain showed neocortical and cerebellar neuronal loss,astrocytosis, and spongiosis (figure A). PrP immunoreactivity showed apunctate pattern and paralleled spongiform changes (figure B). The cat'sbrain showed mild and focal spongiosis in deeper cortical layers of all fourlobes (figure C), vacuolated cortical neurons (figure D), and mildastrogliosis. The cerebellar cortex and the dentate nucleus were gliosed.Immunoreactive PrP showed a punctate pattern in neocortex, allocortex, andcaudate nucleus (figure E). Western blot analysis of control and affectedhuman and cat brain homogenates showed 3 PrP bands of 27-35 kDa. Afterdigestion with proteinase K and deglycosylation, only samples from theaffected patient and cat showed type-1 PrPres, with PrP glycoform ratioscomparable to those observed in sporadic CJD1 (details available fromauthor). [Image] Microscopic sections of patient and cat brains A: Occipital cortex of the patient showing moderate spongiformdegeneration and neuronal loss (haematoxylin and eosin) and B: punctateperineuronal pattern of PrP immunoreactivity; peroxidaseimmunohistochemistry with monoclonal antibody 3F4. C: cat parietal cortexshowing mild spongiform degeneration (haematoxylin and eosin).D:vacuolated neurons (arrow, haematoxylin and eosin), E: peroxidaseimmunohistochemistry with antibody 3F4 shows punctate perineuronaldeposition of PrP in temporal cortex. This study shows a spatio-temporal association between human and felineprion diseases. The clinical features of the cat were different frompreviously reported cases of FSE which were characterised by gradual onsetof behavioural changes preceding locomotor dysfunction and ataxia.5Neuropathological changes were also at variance with the diffuse spongiosisand vacuolation of brainstem neurons, seen in FSE.5 The synaptic pattern ofPrP deposition, similar in the cat and in the patient, was atypical for aBSE-related condition. Evidence of a new type of FSE was further provided bythe detection of a type-1 PrPres, other than the BSE-associated type 4.2Taken together, our data suggest that the same agent strain of sporadic CJDwas involved in the patient and in his cat. It is unknown whether these TSE occurred as the result of horizontaltransmission in either direction, infection from an unknown common source,or the chance occurrence of two sporadic forms.

1 Parchi P, Castellani R, Capellari S, et al. Molecular basis of phenotypicvariablity in sporadic Creutzfeldt-Jakob disease. Ann Neurol 1996; 39:767-78 [PubMed]. 2 Collinge J, Sidle KCL, Meads J, Ironside J, Hill AF. Molecular analysis ofprion strain variation and the aetiology of 'new variant' CJD. Nature 1996;383: 685-90 [PubMed]. 3 Bruce ME, Will RG, Ironside JW, et al. Transmissions to mice indicate that'new variant' CJD is caused by the BSE agent. Nature 1997; 389: 498-501[PubMed]. 4 Hill AF, Desbruslais M, Joiner S, et al. The same prion strain causes vCJDand BSE. Nature 1997; 389: 448-50 [PubMed]. 5 Pearson GR, Wyatt JM, Henderson JP, Gruffydd-Jones TJ. Feline spongiformencephalopathy: a review. Vet Annual 1993; 33: 1-10.
------------------------------------------------------------------------
Sezione di Neurologie Clinica, Dipartimento di Scienze Neurologiche e dellaVisione, Università di Verona, Policlinico Borgo Roma, 37134 Verona, Italy(S Monaco; e mail [email protected]); and Istituto ZooprofilatticoSperimentale della Lombardia e dell' Emilia, Brescia
=========================================TSS
indeed there have been 4 documented cases of TSE in Lions to date.
Lion 32 December 98 Born November 86
Lion 33 May 1999 (euthanased) Born November 81.
Lion 36 Euthanased August 2000 Born July 87. Deteriorating hind limb
ataxia.
Lion 37 Euthanased November 2001 Male, 14 years. Deteriorating hind
limb ataxia since September 2001. (Litter mate to Ref. 36.)
http://www.defra.gov.uk/animalh/bse/index.html
go to the url above, on the bar at the top, click on _statistics_,
then in middle of next page, click on_other TSEs_.
or go here;
http://www.defra.gov.uk/animalh/bse/bse-statistics/level-3-tsestat.html:

and
http://www.defra.gov.uk/animalh/bse/bse-science/level-4-othertses.html:

http://www.bseinquiry.gov.uk/files/yb/1992/11/13001001.pdf:

also;
Reports on the clinical symptoms presented by these cats give a
relatively homogeneous picture: Affected cats show a lack of
coordination with an ataxia mainly of the hind limbs, they often fall
and miss their target when jumping. Fear and increased aggressiveness
against the owner and also other animals is often seen. They do not
longer tolerate to be touched (stroked) and start hiding. These
behavioural chances might be the result of a hypersensibility to touch
and noise, but also to increased fear. Excessive salivation is another
more frequently seen symptom. Cats with FSE in general show severe
behavioural disturbances, restlessness and depression, and a lack of
coat cleaning. Symptoms in large cats in general are comparable to those
in domestic cats. A
report on FSE (in german) has been presented in 2001 in the Swiss FVO
Magazin. A paper on the first FSE case in a domestic cat in Switzerland
is currently in press in the Journal Schweizer Archiv für Tierheilkunde
(SAT).
http://www.neurocenter-bern.ch/tse_e.shtml:


TSS
 
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