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From: TSS ()
Subject: Neuropathological findings in cats with clinically suspect but histologically unconfirmed feline spongiform encephalopathy
Date: April 20, 2005 at 10:41 am PST

-------- Original Message --------
Subject: Neuropathological findings in cats with clinically suspect but histologically unconfirmed feline spongiform encephalopathy
Date: Tue, 19 Apr 2005 14:13:32 -0500
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy

##################### Bovine Spongiform Encephalopathy #####################

The Veterinary Record, April 9, 2005
AGAINST the background of bovine spongiform encephalopathy
(BSE) in the UK in the late 1980s, the diagnosis of a
small number of cases of a closely similar disease, termed
feline spongiform encephalopathy (FSE), in domestic cats
(Leggett and others 1990,Wyatt and others 1990, 1991, Synge
and Waters 1991) raised public concern about the possibility
of an epizootic of a transmissible spongiform encephalopathy
(TSE) in this species. This concern has not been borne out
by experience; up to November 30, 2003, 89 cases of FSE have
been confirmed in Great Britain and the Channel Islands,
compared with 180,324 cases of BSE (DEFRA 2004).
Furthermore, the epizootic of FSE had declined markedly since
1994, with only single cases being recorded in the years 1998
to 2001 and no cases in 2002 or 2003 (J.W.Wilesmith, G. A.
H.Wells, unpublished observations).
In 1990, however, the State Veterinary Service (SVS) published
advice to veterinary surgeons about the clinical and
neuropathological investigation of cats with neurological disease
which gave rise to a suspicion of FSE (Meldrum 1990).
At that stage the SVS undertook to screen the brains of clinically
suspect cats for the presence or absence of neurohistological
lesions of FSE. In addition, with veterinary surgeons
alerted to the potential diagnosis, a few cats were referred to
university veterinary schools, either for clinical investigation
or for postmortem examination. Between 1990 and 1997 over
270 cats were submitted by private veterinary surgeons,
mainly to the SVS, principally for this screening. In addition
to the cats with confirmed FSE, there were other clinically suspect
animals in which FSE was excluded on the basis of a neurohistological
examination. This paper summarises the results
of the examination of 192 of these latter cases; preliminary
observations have been described by Kelly and others (1997).
Source of material
Cats with neurological signs for which the differential diagnosis
could have included FSE were submitted, after they had
been euthanased, to regional laboratories, formerly veterinary
investigation centres (VICs) of the Veterinary Laboratories
Agency (VLA), or to the former Central Veterinary Laboratory,
with their signalment, age and clinical details summarised
on a standard form (Franklin 1997). A few such cases were
referred from university veterinary schools or from private
veterinary laboratories to the VLA as pathological material. All
the submissions were voluntary. In 1994, however, the diagnosis
of FSE or any spongiform encephalopathy in species
other than cattle, sheep and goats became notifiable, but only
on laboratory confirmation (Anon 1994). The data on all the
submissions were collected, and cases of FSE were confirmed
and notified to the SVS headquarters through laboratory
referral, ultimately to VLA  Weybridge.Material from one of
the suspect FSE cases came from Norway; it was referred in the
light of a previously confirmed case from that country
(Bratberg and others 1995). All the other cases were from
Great Britain.
At the regional laboratories, the brain and, in some cases, the
cervical spinal cord of the cats was removed and fixed in 10
per cent neutral buffered formalin. The fixed brains were
initially examined macroscopically by one of the authors
(R. J. H., M. J. or G. A. H.W.). Blocks of brain (usually cerebrum,
cerebellum, mesencephalon and medulla) and, when
available, spinal cord were processed histologically to paraffin
wax by standard methods, and sections were stained with
haematoxylin and eosin and examined microscopically (by R.
J. H., M. J. or G. A. H.W.).When the material did not originate
from a submission to a regional laboratory, formalinfixed
central nervous system (CNS) samples, principally brain,
were received as either wet tissue, paraffin-wax blocks and/or
sections stained with haematoxylin and eosin, and were
examined similarly.All the sections were reviewed separately
by D. F. K. without knowledge of the initial diagnosis.When
all the sections had been reviewed the collected observations
were tabulated by D. F. K. and G. A. H. W. Histological
descriptions of the CNS sections were interpreted by reference
to standard veterinary neuropathology publications (Innes
and Saunders 1962a, b, Luginbühl and others 1968, Summers
and others 1995 a to f, Koestner and others 1999).
Immunostaining for PrPSc
Paraffin-wax sections of brain from 173 of the 192 cases were
examined immunohistochemically for the presence of PrPSc,
the disease-specific form of the prion protein and a marker
for all TSEs. The sections were dewaxed, dehydrated and autoclaved
in water at 121°C for 30 minutes (Haritani and others
Veterinary Record (2005)
156, 472-477
D. F. Kelly, MA, PhD, BVSc,
Department of Veterinary
Pathology, Faculty of
Veterinary Science,
University of Liverpool,
Crown Street, Liverpool
L69 7ZJ
G. A. H.Wells, BVetMed,
M.Haritani, DVM, PhD,
Veterinary Laboratories
Agency  Weybridge,
New Haw, Addlestone,
Surrey KT15 3NB
R. J.Higgins, MSc,
Veterinary Laboratories
Agency  Thirsk,West
House, Station Road,
Thirsk, North Yorkshire
M. Jeffrey, DVM, BVMS,
Veterinary Laboratories
Agency  Lasswade,
Pentlands Science Park,
Bush Loan, Penicuik,
Midlothian EH26 0PZ
Dr Haritanis present
address is National
Institute of Animal
Health, Tsukuba, Ibaraki,
305-0856, Japan
Mr Higginss present
address is Veterinary
Laboratories Agency 
Lasswade, Pentlands
Science Park, Bush Loan,
EH26 0PZ
Neuropathological findings in cats with
clinically suspect but histologically
unconfirmed feline spongiform
D. F. Kelly, G. A. H. Wells, M. Haritani, R. J. Higgins, M. Jeffrey
Central nervous system (CNS) tissues from 192 cats with neurological
signs were examined histologically,
and tissues from 173 of them were later examined immunohistochemically
as part of a survey to determine
the prevalence of feline spongiform encephalopathy (FSE). One of the
cats was from Norway and the others
were from Great Britain. The most commonly recorded clinical signs were
ataxia, behavioural changes and
epilepsy, but none of the cats had histopathological evidence of FSE.
The most common organic CNS lesions
were non-suppurative encephalomyelitis in 28 per cent, neoplasia in 15
per cent and a heterogeneous group
of degenerative encephalopathies in 9 per cent of the cats. A range of
minor histological lesions of uncertain
significance was also observed. No histological lesions were observed in
the tissues of 63 (33 per cent) of
the cats. Disease-specific prion protein (PrPSc) was observed in only
one of the 173 cats examined by
Papers & Articles
The Veterinary Record, April 9, 2005
1994). The primary anti-PrP monoclonal antibody 3F4
(Kascsak and others 1987) was applied at dilutions of 1:8000
and 1:16,000 for 20 hours at 4°C in an avidin-biotin-peroxidase
complex technique. The sections were counterstained
with Mayers haematoxylin. Immunostaining was controlled
by omission of the primary antibody. The immunostained
sections were examined by brightfield light microscopy for
the disease-specific configurations of PrPSc previously determined
for domestic cats with FSE using the 3F4 antibody
(Wells and others 1994, Bratberg and others 1995).
Clinical observations
The clinical signs recorded are listed in Table 1. The cats were
referred primarily by veterinary surgeons in general practice
and detailed neurological investigation was not part of the
survey. Clinical signs were not always recorded and other
information was often incomplete.The ages of only 139 of the
192 cats were recorded; 130 of these were more than a year
old,with a range from one-and-a-half to 18 years and a mean
of 7·47 years, and the others ranged in age from three to 11
Neurohistological observations
The broad categories of histological observations for the 192
cats are listed in Table 2; they are not, in themselves, contentious
and only abbreviated descriptions are given.
Non-suppurative meningoencephalitis In 36 of the cats
the changes were characterised by a constellation of common
microscopic features: perivascular cuffing by lymphocytes
and plasma cells, variably involving meningeal and deep brain
capillaries (Fig 1), which was accompanied by focal microgliosis
of variable distribution and severity.These microscopic
features were collectively described as non-suppurative
meningoencephalitis, not otherwise specified (NSME, NOS); in
a few of these cats this pattern of inflammatory reaction had,
in addition, focal or more diffuse gemistocytosis (Fig 2). A
variation on NSME, NOS, observed in 17 cats, included, in addition,
a range of ependymal, choroid plexus and meningeal
arterial changes: fibrinoid necrosis of the tunica media,
perivascular exudation of fibrin, neutrophilic leucocytes and
macrophages, fibrosis of the tunica intima and focal splitting
of the internal elastic lamella (Figs 3 to 5). In some cats the
inflammatory reaction involved a large proportion of plasma
cells. This variant of NSME was referred to as NSME, FCV (putatively
associated with reaction to infection by feline coronavirus).
Degenerative encephalopathies These include morphologically
heterogeneous lesions in which primary degenerative
changes were found at different anatomical sites (Table
The most common lesion in this category was laminar
cerebrocortical degeneration, which affected nine cats. This
term was used to describe a range of lesions that extended
from laminar neuronal ischaemic change through to distinct
laminar cortical malacia (Fig 6), incipient cavitation and a
marked associated gliomesodermal reaction. Leucomalacia
refers to rarefaction and cavitation of cerebral subcortical
white matter, usually with a marked gitter cell reaction. In
other examples included in this group there were degenerative
foci involving neuronal loss, gitter cell infiltration and
gliomesodermal proliferation.
Neoplasia Twenty-eight of the cats had neoplastic brain
lesions; in descending order of frequency the most common
tumours were meningioma, lymphosarcoma and astrocytoma
(Table 4). The meningiomas were well circumscribed,
nodular and compressive tumours situated most commonly
on the external meningeal surface of the brain, or in the
Papers & Articles
Signs recorded Number of cats
Ataxia 61
Behavioural changes* 31
Epilepsy 18
Circling/head pressing 5
Head tilt 5
Blindness 2
Paresis/paraplegia 1
* Personality change, aggression, hyperaesthesia
As recorded and presumed to refer to episodic seizures
TABLE 1: Neurological signs recorded in 123 cats in a survey for
feline spongiform encephalopathy in Great Britain
Neurohistopathological category Number of cats
Non-suppurative meningoencephalitis (NSME) 53
(NSME, NOS* 36)
(NSME, FCV 17)
Degenerative encephalopathies 18
Neoplasia 28
Other lesions 30
No histological abnormality 63
* NSME, not otherwise specified
NSME consistent with reaction to feline coronavirus infection
TABLE 2: Categories of neurohistopathological findings in 192
cats examined in a survey for feline spongiform
encephalopathy in Great Britain
FIG 1: Example of
not otherwise specified,
showing multifocal
pericapillary cuffing
by lymphocytes.
Haematoxylin and
eosin. x 150
FIG 2: Example of non-suppurative meningoencephalitis, not
otherwise specified, showing pericapillary cuffing with
lymphocytes and plasma cells, and adjacent gemistocytosis
(arrows). Haematoxylin and eosin. x 500
The Veterinary Record, April 9, 2005
supraventricular connective tissue of tela choroidea (Fig 7).
In contrast, the lymphosarcomas consisted of poorly demarcated
multifocal infiltrations of the meninges and neuropil by
neoplastic lymphoid cells (Fig 8). The astrocytomas were illdefined
infiltrative cerebral tumours consisting of large angulated
cells with plentiful pale eosinophilic cytoplasm and large
round or pleomorphic hyperchromatic nuclei (Fig 9); necrosis
and haemorrhage were common features of astrocytomas.
The single examples of carcinoma and fibrosarcoma were presumed
to be metastatic, but no further comment is possible
in the absence of more detailed clinical data and due to
incomplete postmortem examinations.
Other lesions These included a heterogeneous group of
microscopic lesions that did not fit into any of the previous
morphological categories (Table 5). Myelinopathy describes
the presence of focal swelling of the myelin sheath, accompanied
by gitter cell reaction (Fig 10). Meningeal vasculosis
describes focal fibrinoid degeneration of the meningeal
arterial tunica media, sometimes associated with eccentric
fibrous thickening of the tunica intima.
Four cats had acute inflammation of the brain, spinal cord
or meninges, with copious fibrinous exudate and myriad
neutrophilic leucocytes (Fig 11). These lesions were thought
likely to be of bacterial origin, but the CNS was not cultured.
Two young cats, aged four and nine months, had a neuronal
storage disease characterised by cellular swelling with cytoplasmic
granular vacuolation (Fig 12).No attempt was made
to define the chemical nature of the storage product or the
putative lysosomal enzyme abnormality.
None of the 192 cats had the histological changes characteristic
of spongiform encephalopathy.
PrPSc immunohistochemical observations Of the 173
neurohistologically negative cases examined, disease-specific
PrPSc immunostaining was detected in only one brain. This
cat was recorded as having neurohistological changes only of
focal dural mineralisation, categorised under other miscellaneous
lesions (Table 5).However, there was artefactual disruption
of the brain parenchyma, characteristic of freezing
and thawing before primary fixation, and this may have
obscured any changes due to FSE.
The authors emphasise that the material on which this survey
is based was obtained with limited objectives; first, to determine
the prevalence of spongiform encephalopathy in domestic
cats in Great Britain, and secondly, to reassure the cats
owners when the neurohistological examination confidently
excluded FSE as a cause of the neurological disease. A detailed
clinical examination by veterinary neurologists was not part
of the survey, so the clinical signs recorded (Table 1) are likely
to have been those most obvious to non-specialised small
animal clinicians. Ataxia and behavioural changes were the
neurological abnormalities recorded most commonly, just as
they are among the most common clinical signs of FSE (Wyatt
and others 1990, 1991, Leggett and others 1990).However, the
incompleteness of the records of the signalment and clinical
signs limited a critical analysis and any correlation of the
neurological signs with the neuropathological findings. In
some cases the neurological signs should not have led to a
strong suspicion of FSE, for example, in the two young cats
with a neuronal storage disease (Table 5, Fig 12).
Papers & Articles
FIG 3: Example of non-suppurative meningoencephalitis
consistent with reaction to feline coronavirus infection:
cerebrum showing extensive plasma cell accumulation in
connective tissue of the choroid plexus. Haematoxylin and
eosin. x 500
FIG 4: Example of
consistent with reaction
to feline coronavirus
infection: medulla
showing extensive
meningeal fibrinous
infiltration and
perivascular cuffing in
adjacent neuropil.
Haematoxylin and
eosin. x 200
FIG 5: Example of non-suppurative meningoencephalitis
consistent with reaction to feline coronavirus infection:
medulla, showing a small meningeal artery with eccentric
intimal fibrinous exudation, focal medial fibrinoid necrosis
with medial and adventitial infiltration by neutrophilic
leucocytes and lymphocytes. Haematoxylin and eosin. x 250
FIG 6: Cerebrum
showing laminar
cortical malacia
with adjacent
reaction. Haematoxylin
and eosin. x 150
The Veterinary Record, April 9, 2005
The mean age of the cats whose age was recorded was 7·47
years, which is similar to the average age of seven years of 81
cats with FSE confirmed during the period of the present study
(J.W.Wilesmith, personal communication). A critical comparison
of the cats ages is limited by the incompleteness of
the recorded ages and by the lack of precision about their
actual ages, because accurate dates of birth were often
The categories of neurohistological lesions are summarised
in Table 2, and show that the three most common were
NSME, a range of degenerative encephalopathies and CNS neoplasia.
This distribution of organic brain disease is similar to
that recorded in a series of 30 cats with progressive neurological
disease (Quesnel and others 1997). The most common
pattern of NSME, NOS, characterised by multifocal microgliosis
and pericapillary lymphoplasmacytic cuffing, was designated
NOS (not otherwise specified) and is a pattern of
inflammation assumed likely to have been a response to viral
infection (Vandevelde and Braund 1979, Lundgren 1992). In
recent years this pattern of NSME in some cats has been associated
with infection by Borna disease virus (Lundgren and
others 1995, Nowotny and Weissenböck 1995, Reeves and
others 1998), but no aetiological investigation was attempted
in the present survey. The other pattern of NSME, FCV, had, in
addition, striking inflammatory exudation and vasculopathy
involving both meninges and ependyma. This histopathological
pattern is seen in the CNS of cats with naturally occurring
feline infectious peritonitis (Slauson and Finn 1972,
Summers and others 1995b) and in cats infected experimentally
with feline coronavirus (McArdle and others 1995), and
this variant of NSME was assumed to have resulted from that
specific infection.
The non-diagnostic term degenerative encephalopathies
has been used to include histopathologically heterogeneous
lesions (Table 3), of which laminar cerebral degeneration was
the most common. This latter designation covers a range of
lesions from laminar cerebrocortical neuronal ischaemic
change to cystic cavitation (Fig 6). This pattern of lesions is
consistent with an energy-deprivation injury and can result
from diverse causes, including reduced cerebral perfusion,
hypoxia and hypoglycaemia (Summers and others 1995c).
The limited clinical histories and antemortem data, the
incomplete postmortem examinations and the lack of a systematic
gross examination of the brain all militated against a
critical investigation of the pathogenesis and a detailed neuroanatomical
localisation of these lesions. It is possible that
some of the other lesions in the broad category of degenerative
encephalopathies (Table 3) were within the range of feline
ischaemic encephalopathy (Summers and others 1995d), but
Papers & Articles
Lesion Number of cats
Laminar cerebrocortical degeneration 9
Cerebral leucomalacia 3
Medulla: symmetrical focal malacia 1
Midbrain: focal malacia 1
Cerebrum: subcortical cyst 1
Multifocal poliomalacia: midbrain, medulla 1
Cerebrum: focal neuronal degeneration 1
Colliculus: focal malacia 1
TABLE 3: Degenerative encephalopathies recorded in 18 cats
examined in a survey for feline spongiform encephalopathy in
Great Britain
Neoplasm Number of cats
Meningioma 10
Lymphosarcoma 8
Astrocytoma 7
Oligodendroglioma 1
Carcinoma 1
Fibrosarcoma 1
TABLE 4: Neoplastic lesions recorded in 28 cats examined in a
survey for feline spongiform encephalopathy in Great Britain
FIG 7: Cerebral
meningioma in the
connective tissue of the
tela choroidea, showing
focal calcification
(arrow). Haematoxylin
and eosin. x 150
FIG 8: Cerebrum with
showing diffuse
infiltration of meninges
and neuropil by
neoplastic lymphoid
cells. Haematoxylin and
eosin. x 150
FIG 9: Cerebral
astrocytoma showing
large pleomorphic
tumour cells with
eccentric nuclei and
plentiful eosinophilic
Haematoxylin and
eosin. x 500
Lesion Number of cats
Focal myelinopathy 7
Meningeal vasculosis 4
Vascular mineralisation 3
Suppurative encephalitis/myelitis 2
Suppurative meningitis 2
Focal microgliosis 2
Neuronal storage disease 2
Miscellaneous* 8
* Single examples of focal dural mineralisation, meningeal fibrosis,
focal gliomesodermal reaction, perivascular hyaline, focal
gemistocytosis, axonal swelling, haemorrhagic myelomalacia and
focal vacuolation of neuropil
TABLE 5: Other microscopic lesions recorded in cats examined
in a survey for feline spongiform encephalopathy in Great
The Veterinary Record, April 9, 2005
no further comment can be made owing to the limited background
provided by the objectives of the survey. Focal
myelinopathy refers to patchy swelling of the myelin sheath,
vacuolation and gitter cell reaction (Fig 10). Similar white
matter lesions were common as part of the neuropathology
observed in a series of mainly laboratory-maintained young
cats by Palmer and Cavanagh (1995),who speculated that the
cause could be viral.
The range of neoplasms observed (Table 4) was similar to
the range observed in current clinical and pathological experience
in cats, in which meningioma is the most common
primary brain tumour (Whitehead 1967, Engle and Brodey
1969, Hayes and Schiefer 1969, Summers and others 1995e).
Involvement of the CNS by lymphosarcoma was also common
(Summers and others 1995f), in agreement with earlier observations
from a university small animal hospital with a large
referred cat practice (D. F. Kelly, unpublished observations).
It was assumed that the single examples of carcinoma and
fibrosarcoma were likely to have been metastatic, but their
primary sources were not identified either from the clinical
history or from the partial postmortem examinations.
The range of other histological changes (Table 5) included
some lesions, for example, suppurative encephalitis/meningitis,
neuronal storage disease and haemorrhagic myelomalacia,
that are likely to cause neurological signs.Many of the
other abnormalities were minor focal lesions that were probably
incidental and would have been unlikely to cause clinical
A striking feature was the large proportion of the cats in
which no histological abnormalities were observed in the CNS
(Table 2). There are two possible explanations for this observation:
first, the anatomical sampling may not have included
areas of neuraxis that contained morphological abnormalities;
and secondly, there may have been no morphological
substrate for the neurological signs, which might have
resulted from functional neurotoxic effects mediated by access
to environmental neurotransmitters. Testing of these speculative
explanations is again severely limited by the nature of
the survey.However, the unexplained neurological signs were
similar to observations in other cats with progressive neurological
disease (Quesnel and others 1997, D. F. Kelly, unpublished
The results of this survey show that, against a background
of 81 cases of FSE diagnosed histopathologically in Great
Britain between May 1990 and December 1997 (MAFF 1998),
129 of 192 cats with neurological signs had a range of organic
CNS lesions, of which the three most common were non-suppurative
meningoencephalitis of putative viral aetiology, primary
and secondary brain tumours, and a range of
degenerative encephalopathies of uncertain aetiology. The
other 63 cats had no histological abnormalities in the CNS tissues
examined. In only one of 173 of the cats in which the
brain was examined immunohistochemically was there evidence
of disease-specific PrPSc, and in this animal the absence
of the characteristic changes of FSE could not be assessed
because of a histological artefact.
These observations illustrate not only the value of surveillance
for the detection of one specific disease entity but
also that such surveys may reveal a wider range of lesions than
initially envisaged. In this respect the variety of CNS lesions
observed was reminiscent of the lesions revealed by the
histological examination of cattle brains in the course of
surveillance of animals showing clinical signs that might have
been associated with BSE (McGill and Wells 1993).
Since this manuscript was accepted for publication a similar
paper has been published (Bradshaw and others 2004). Those
authors reviewed archived CNS tissue from cats that had neurological
signs and had been referred to the University of
Bristol during the period 1975 to 1998. The review listed a
range of neuropathological lesions: congenital (n=12); degenerative
(n=42); dysautonomia (n=27); inflammatory (n=92);
neoplasia (n=38); spongiform encephalopathy (n=24); and
no lesions were found in 51 cats. This study, based on a veterinary
school database, is therefore complementary to the
findings summarised here.
The authors thank the many veterinary surgeons in private
practice who referred the cats, the staff of the former VICs who
Papers & Articles
FIG 11: Edge of a
brain abscess, with
encephalitis showing
malacic cavitation and
diffuse infiltration by
neutrophilic leucocytes.
Haematoxylin and
eosin. x 300
FIG 12: Medulla of a four-month-old kitten with putative
lysosomal storage disease, showing swollen, vacuolated
neuronal cytoplasm. Haematoxylin and eosin. x 300
FIG 10: Medulla with focal myelinopathy, showing swelling
and vacuolation of myelin sheaths and reactive gitter cells.
Haematoxylin and eosin. x 300
The Veterinary Record, April 9, 2005
collected and processed the material, particularly at VIC
Thirsk, where much of the histological processing was undertaken,
and the staff of the Histopathology Unit and the
Neuropathology Section, VLA  Weybridge, for skilled technical
work. The task of correlating the case data was ably
accomplished by Mrs Sally Franklin, formerly of the
Neuropathology Section, VLA  Weybridge. The authors also
thank Dr Richard Rubenstein, Institute for Basic Research in
Development and Disabilities, Staten Island, New York, USA,
for the gift of the 3F4 antibody. The work was funded by the
former Ministry of Agriculture, Fisheries and Food.
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Papers & Articles


wonder what would have been found if Western Blot with the addition of
phospohtungstic acid
precipitation step (Bio-Rad Deslys et al) and or the CDI Prusiner
et al are boasting about were used on these cats???


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