Second International Feline Coronavirus & Infectious Peritonitis
Symposium - a report by Jen Lacey

The Second International Feline Coronavirus / Feline Infectious
Peritonitis Symposium was held in Glasgow, Scotland, UK 4-7 August
2002. Like the hugely successful first FECV/FIP Workshop hosted by
Prof. Niels Pedersen in UC Davis, the second welcomed scientists,
Veterinary surgeons, cat breeders, cat rescue charities and industry.
Prof. Niels Pedersen began the meeting by giving an overview of Feline
Coronavirus and Feline Infectious Peritonitis. The conference co-
ordinator was Dr Diane D. Addie. The proceedings will be published in
the Journal of Feline Medicine and Surgery.
Scientific committee: Prof. Niels Pedersen, Prof. Hans Lutz, Prof.
Marian Horzinek, Prof. Oswald Jarrett, Dr Diane D. Addie. Local
organising committee, Dr Diane D. Addie, Prof. Oswald Jarrett, Dr
Margaret Hosie.

The Beginning
The Scottish welcome was very warm, with a ceilidh, haggis, kilts and
pipers, plus the wee dram, of course, all contributing. Whilst most
other parts of the UK seemed to be having torrential downpours or heavy
mist, we were bathed in warm sunshine . There was the little matter of
cryptospiridium in the water supply, but nothing to panic veterinary
scientists! These had come from all parts of the world. Australia,
Japan, Australia and South Africa were represented, as well as North
America, many European countries and the UK. It was satisfying to put
faces to some well known names, Dr Neils Pedersen, Dr Janet Wolf, and
Dr Susan Little were there; and it was good to meet in person, Dr Diane
Addie of Glasgow University who had co-ordinated the event, but mostly
because she was taking a special interest in the FIP outbreak amongst
my own cats and kittens. Over the 3 days the Symposium had 4 main
sessions presenting papers on: Diagnosis & treatment of FIP,
Epidemiology of FCoV Infection, Pathogenesis & Immunopathogenesis of
FIP and Prevention of FcoV Infection/FIP. They were preceded by two
speakers who gave a history of the study of the disease (Pedersen) and
what it's like to actually live with an FCoV household (Sue Perry from
Sleaford, whose tribe were all rescues of the sort nobody else would
take on). On the final afternoon we broke for workshops, on
'Diagnosis', 'Minimising Disease Spread', or 'Recommendations for
Future Research'. One of my reasons for being there was to learn all I
could from the second and it was a stimulating afternoon. Taking the
event as a whole though, I can't say there was much cause for celebration. That had absolutely nothing to do with the quality of the
speakers or the presentations. I suppose the tone was set by Dr
Pedersen in his introduction when he told us that the disease had been
named in 1963 and fully described by scientists from Cornell in 1966.
We also saw a slide of a photo taken in 1912 that showed a little cat
with the typical swollen abdomen of the effusive form of FIP, so it's
something that's known to have been around for a long time. He defined
FIP as an important cause of death for young cat from catteries and
shelters, but said that the years of study had not yet brought any easy
way to prevent the disease and no way at all to cure it. He also
admitted some blind alleys. The worst of which was the publication of a
paper in the 70s which indicated FIP could be detected from an antibody
titre test. Unfortunately, there was a weakness in the study as no
comparison had been made with cats in multicat households (MCH). Within
quite a short the data was available and corrections made, but still
today probably more cats are euthanised because of a positive FcoV
antibody titre than die of FIP. So prevention difficult, with the only
available vaccine in no way helpful to those who most need it, kittens
of 8+ weeks who have already been exposed to the virus in their MCH or
shelter, and no cure. All the years had brought was a lot greater
understanding. The research presented at the Symposium would add to
that, and there were a couple of gleams of light from beyond the
boundaries of feline medicine as both mouse hepatitis and dengue fever
(human) developed and progressed as FIP did in cats, so studies of
these could contribute. He had hoped FIP would reduce as FeLV was
effectively beaten, but it had made no significant difference. As yet
then only a hard road ahead. I'll try tomorrow to give more detail of
those studies I found most interesting, and then I'll describe the
conclusions of the workshop on what we as breeders could do. I've pages
of notes, but big lashings of info without the pictures and diagrams
that went in to illustrate aren't that digestible.

Breeder Study
Kinetics of FCoV Infection in Kittens Born in Catteries of High Risk
for FIP Under Different Rearing Conditions - Lutz H. et al, University
of Zurich. This was a significant paper for me as on the day it was
given my litter born to a queen with a high titre (she was newly
pregnant as FIP was diagnosed in my cattery) were three weeks old. Dr
Addie's recommendation was that I should separate the kittens from
their mother at five weeks (early weaning) in an attempt to prevent
them becoming infected with FCoV. I had reservations, not because the
actual weaning process would be difficult, but because the maternal
bond in Korats is strong and queens continue to be protective and
caring for their kittens at least twice as long as this, thus playing a
significant role in their socialisation. However, I wanted to do all I
could to protect them from FIP so I went to the Symposium really torn
and hoped to get information to help me reach a decision. The purpose
of the study was to determine the course and viral load of natural FcoV
infection in conventionally and early weaned kittens and to consider
the role of vaccination in those who were seronegative. 18 breeders
took part. All were highly motivated as they had a history of FIP in
the past and wanted to do all they could to prevent it. Their selection
was on these 2 criteria. 226 kittens in 63 litters were studied, with
half early weaning and the other raised with their mother and (later)
other cats of the household in conventional fashion as a control group.
FCoV shedding in the faeces of the kittens started as early as 2 weeks
whether the queens were quarantined with their kittens or not. By week
4 20%, and by week 6 50% of kittens tested positive. At this point the
conventionally raised kittens were shedding significantly more FcoV
than the early weaned, but at the age of 9 weeks, and 12 weeks, the
levels were the same for both groups. The two groups were followed for
a total of 21 months. At this point 9 of the kittens had died from FIP.
5 were from the conventionally raised group and 4 from the early
weaned. It was concluded that although the early weaning prevented a
high viral load at a young age it was not found able to keep kittens
free of FCoV infection under field conditions. The vaccination part of
the trial was not followed through as no kittens in the study were FcoV
negative. Of course Dr Lutz was asked if he could produce any reason
for the different results in his trial to Dr Addie's. The size of the
catteries in terms of numbers and space was considered. Dr Lutz
wondered if we all had bigger homes in UK and were more able to
separate cats effectively to prevent contamination of the isolation
necessary for early weaning. Dr Janet Wolf said that in the trials she
had conducted with breeders in USA none had been able to produce FcoV
negative kittens by this method, and Dr Pedersen said that even under
the strictest lab conditions it was difficult not to introduce FCoV to
a clean area, he'd had it happen.Dr Gunn-Moore(Edinburgh) and one of
the Europeans (who also added that she came from a small country
confirmed success for the method. Considering again, Dr Lutz believed
that the answer could well lie with the queens. They were all
significant virus shedders, which correlated strongly with high antibody titres. Dr Addie' groups hadn't been selected on this basis,
and it was agreed she had reported lack of success with some litters
from high titre dams. This report made my own choice harder than ever.
Dr Addie hoped very much that it hadn't put me off trying to early
wean, and I had to admit concern that I could be putting mother and
kittens through a stressful situation for little gain. By the end of
the conference I'd decided on a compromise. Yesterday I sent faeces and
a blood sample from Shula (dam) and faecal swabs from the kittens off
to Glasgow. I should then know whether Shula's titre has decreased
significantly in her 11 week isolation period, and discover whether or
not she's shedding virus at this point in time. I shall also know whether or not the kittens have already been infected from whether
there is evidence of the virus in their samples. If it happens that
their mother is positive and they are clear then I shall separate them
in an effort to protect them.. However, I do it with the knowledge of
the virulence of the virus that infected my cats, I'm not saying that
it's a must for all, and indeed this particular paper shows that it's
just about impossible to achieve the desired result when starting with
cats at high risk of producing kittens, some of whom will go on to
develop FIP (about 4%).

I think these papers deserve a report, but I must admit it was rather
tough going. The most breeder relevant bit is in the final paragraph so
skip to that if you're not wrestling with the is it/isn't it stage of
FIP. I can't give those of you with specialist knowledge much detailed
information on this subject as I'm not a scientist. I picked up on the
fact that when effusion exists and fluid can be extracted it's not too
difficult to come to a diagnosis of FIP, taking the other clinical
signs into account. What would be useful for clinicians is a diagnostic
to rule out FIP in its dry form so that further investigation could
then go on to decide what the actual problem was. It was encouraging to
find when chatting to other delegates socially that several of them
were there from firms who had not yet worked on this to see if it was
worth putting money into the development of diagnostic tests. I hope
they returned home keen and eager. The first paper was AGP Measurement
as an Aid to the Diagnosis of FIP given by S Duthie of Glasgow
University. AGP is an acute phase protein produced by the liver in
response to inflammation. It was monitored in cats with FIP and
diseases with a similar clinical presentation. It was found that
specific levels were of value in distinguishing field cases of FIP from
look alike conditions. Indeed it was concluded that it was more
efficient than the albumin:globulin measure used at present. It is able
to give results within 36 hours. Further research to be done as this
looked promising. The second study (K Hartmann) compared different
diagnostic tests. In all cases FIP had been confirmed or not by
necropsy and histology. The conclusion was that for cats with effusions
diagnostic tools based on the analysis of the fluid have good
predictive values, but this was impossible in many cases where there
was no effusion. Therefore it was recommended that diagnosis should be
made by the more invasive methods of laparotomy, laparoscopy and organ
biopsy. Several of the vets there confirmed that these were now a
preferred option to get a confirmed diagnosis to rule FIP in or out of
the picture in cases with no effusion. To reinforce the last study
research in Poland (P Kita) on RT-PCR to detect FCoV in blood was
evaluated. The test was found to give false positives, with the
inevitable conclusion that the detection of FcoV sequences in blood by
RT-PCR has a limited value as a method of FIP diagnosis. However,
research done in Utrecht was more upbeat on detection in blood. The RT-
PCR was designed to detect mRNA a genetic element of most, if not all,
field CV strains. The most significant result was that of a group of 49
cats, cats with pathologically proven FIP 94% were positive in the mRNA
PCR, whereas the 12 proven to be non-FIP remained negative (100%).
Finally, and perhaps of most interest to breeders, Dr Addie gave an
evaluation of the Feline Coronavirus Antibody immunocomb. This could be
used as an in-house test for vets. It scored well against the
immunoflorescent antibody tests (84% & 85% for two different readers).
From 110 samples 2 with a 0 titre and 3 with a titre of 1:10 scored
higher indicating that it could give false positives, and cats with a
low positive score would need to be screened in the usual way. However,
no false negatives were recorded, so it was concluded that it could be
used with confidence in for entry into a FcoV stud or cattery.

Treating cats sick with FIP
The outlook is very poor for cats diagnosed to have FIP (by effusion
sample in the wet form, by biopsy in the dry). It's believed that any
said to have recovered probably didn't have FIP in the first place,
particularly as nothing claimed as effective has ever been able to be
repeated in lab conditions. However, recently, since the advent of
veterinary interferon, hopes have been raised that this could at least
put the disease into remission so that cat and owner could enjoy extra
months, if not years, together. The one paper on FIP treatment was from
T Ishida of the Akasaka Animal Hospital, Japan. He reported on an
evaluation of the therapeutic effects of a feline interferon currently
commercially available in Japan, UK and EC. The cases considered were 6
males and 6 females, all FIP diagnosed on 5 counts (they didn't want to
use any animals whose symptoms were vague). A treatment regime was
initiated in which alpha interferon was used in conjunction with
glococortoid treatment (dexamethasone & prednisalone). More detail of
exactly what was given, with the specific amounts is detailed in the
abstract, but I think that anyone wanting their vet to follow the same
path would need to consult with the Japanese institute involved, rather
than anything I copied out. The results were interesting. There was an
age split. 4 of the cats responded to the therapy and have survived
without illness for more than 2 years (though it must be said that full
health and strength did not return). 2 showed a partial response and
survived for 4 months and 5 months. All 6 had effusion initially and
were over 5 years old. The other 6 were 3m-5y.o. or they had no
effusion. On death these were shown to have had FIP by necropsy. So it
was interesting that both age and form of FIP had significance for
recovery. One criticism of this study that came from the floor after
the paper was presented, was that there had been no control group
receiving the glutocortoids only. Other scientists were interested to
know whether prednisalone alone, plus the general treatment, would have
had the same effect. How vital was the interferon? Work for the future

This is the study of the prevalence of a disease, or put another way
Corona Virus, where it's at. None of the papers presented in this
section gave the slightest bit of comfort to me as a breeder. Without
exception it was shown that there are two 'exposure factories' for
FCoV: rescue shelters and pedigree breeders, with other MCHs also
featuring. For instance, 'Operation Catnip' Gainesville, Florida was a
typical, catch, neuter and release of ferals. (Ear tops were clipped to
ensure the same cat didn't get 'done' twice over). Blood sample were
taken from 250 of these to test for the prevalence of a variety of
diseases. A measure of FIP antibodies was just one of a range. Those
involved were surprised to find that only 18% of this group tested
positive for FCoV, and of these 29 cats that did, only 6 had a titre
greater than 1:320. Dr Addie had conducted a much wider study in
Britain of 2,207 cats relinquished to cat rescue shelters. Where
possible she had obtained information of the cat's background. Its sex
didn't make any difference to whether it was sero-positive, the sick
and the young had a slightly greater chance than the healthy and and
the adult. But with a 17% chance overall of being positive, and only an
11% chance for an adult feral, if the cat was designated as a pedigree
or a pedigree x on reception it had a whopping 74% chance of being FcoV
positive. The number of pedigrees taken at the shelters in her survey
even skewed the statistics for the spread of FCoV after arrival and the
subsequent FIP cases, with those taking the greatest numbers having the
worst record, despite husbandry practices being very much the same. Not
feeling too bad yet? Then contrast the findings of Dr Pedersen in
California, where he found of 50 kittens under age weeks of age of
feral/outdoor owned origin coming into a shelter none was FcoV
positive, against Dr Lutz's Swiss study, I detailed earlier, where 226
kittens from 18 catteries were 100% were positive by 8 weeks. OK, these
were breeders who had asked for help because of FIP problems, but in a
second study by Dr Lutz on 132 cats & kittens in 8 catteries 90% were
positive and shedding virus for at least a portion of 24 week period.
Of course we all breathe a sigh of relief as FeCV does not mutate to
become FIP in the overwhelming majority of cases. We are not talking
about an epidemic with cats dropping like flies After all it was only
4% of those in Dr Lutz's study. and in each case the cattery had had
previous FIP cases. Still can't say I'm easy though with conclusions
such as: These data are consistent with the belief that feline corona
infection is primarily a disease of cats that live together in large
groups. Feral cats are an unlikely to be a significant reservoir for
infection with feline corona virus of owned outdoor cats." AM Legendre
(University of Florida) "Since FCoV is transmitted faecal-orally, it
was expected that life-styles which engender more contact of cat s with
the faeces of other cats would predispose to a higher prevalence of
FcoV seropositivity. Feral cats were less likely to be SP than pets or
strays. Pedigree cats were significantly more likely to be SP than
domestic cats, associated with originating from an MCH." D Addie
(University of Glasgow) "FCoV shedding in faeces is widespread in
catteries and represents an important source of FCoV spreading." Lutz H
(University of Zurich). Personally, I don't like being thought of as
one of a group responsible for spreading infection, possible deaths and
the ensuing misery each life lost brings. I shall do my best over the
coming months to put into practice suggestions made at the workshop for
prevention on the last afternoon (I've yet to write up the details,
saving it as a conclusion) and aim to lose no more lives to this. 4 in
every hundred is still too higher price by my reckoning.

I think I've just about reached the last chapter of my reports. I
suppose those I've bombarded with just too much information have
probably switched off by now, but the conference was just about the
steepest learning curve I've been on for a good few years, and I felt I
had to share as much as possible. If there's been a certain sour note
to what I've had to say at times, please remember that my losses to FIP
happened this year and are very fresh in my memory. Just by being there
I rubbed a very sore spot, and some of what I heard had the same effect
as adding vinegar to the wound. This was a self inflicted injury only.
No one I spoke to directly had anything but sympathy for my situation,
and the speakers referring to the high incidence of FCoV in breeding
catteries were doing so to define situations where the MOST HELP was
needed, rather than dishing out condemnation. Those following this most
closely will have realised I've skipped the immunopatholgy and
pathology papers. I was too way out my depth here to be able to
summarise the reports, but I do know the papers gave important new
research detailing how the disease progressed within the cats, which
could help with early diagnosis, and prevention perhaps in the future.
The cell mediated immune response (which is what prevents cats getting
FIP, antibodies don't) is an exciting new area of study. In Utrecht
University they are currently comparing the CMI in cats that either
survived or succumbed to FIP, and when the difference has been under-
stood that should be be a major step forward. Dr Radford is pursuing an
understanding of CMI at Liverpool too, to gain knowledge of specific
genetic predisposition to cope with disease. I mention his study
because DNA from a family of my cats (given when Korats were being
screened for GM) has been used in the study. I took comfort from the
fact that in a very small way I'd contributed something positive.
Before breaking for the workshops on Wednesday there were four papers
on new vaccine approaches, 2 from Utrecht, one from Bristol and the
other from Virbac (France). There were some promising leads that would
be further explored, but Dr Pedersen's view given at the beginning of
the Prevention' session was that we can't just sit around and wait for
a vaccine, because anything new that will be effective for all is most
probably years away. The efficacy, or not, of Primucell wasn't a
discussion topic, so I won't comment either, as I know absolutely
nothing about it (not licensed for use in UK). The only point of note
is that to be of any great use a vaccine should be able to protect
those already exposed to FCoV at an early age, as it's been frequently
demonstrated that it's this group who are at most risk. Primucell makes
no claim to do that. The workshop brief was, "Recommendations for
Minimising Disease Spread in Breeding, Rescue and Boarding Catteries,
In Veterinary Practices and at Cat Shows". The last three we dropped
After a very brief discussion. That's not to say that FCoV cannot be
transmitted from one cat to another at any of these places. Dr Addie's
household study demonstrated that a new virus strain can be introduced
without a known source, but situations where litter boxes are not
shared, and some disinfection procedures are being used, can be
considered low risk. (Incidentally, when Dr Pedersen learnt that our
boarding catteries are inspected and licensed he was most impressed.)
For shelters and rescue centres the key word was HOUSING. No two or
more litters of kittens should share the same accommodation unit at any
time during their stay. The same should also go for foster homes used
by any rescue organisation. Unless separate facilities are available,
one litter at each should be the rule for fostering, and any well
meaning person letting kittens mix should only get one warning (CP
vet). Any available money for expansion, updates etc, then improving
the husbandry facilities of the young should be a priority. As an aside
Dr Pedersen believed that well-meaning people think they're doing
abandoned kittens a favour by taking them to a shelter. If they could
only do, as used to be the case, and find homes for them themselves,
the kittens would have a greater chance of remaining healthy. For
breeding catteries LITTER BOX HYGIENE and NUMBERS were prime
considerations. Keeping litter faeces free, not sharing boxes between
different groups of cats, keeping any scoops, brushes etc specific for
each place; these measures have been discussed several times. As far as
the number of cats for a household was concerned it was considered that
FIVE was enough for any home that did not have facilities to house
separate groups. Two or three in any one group would be ideal to
prevent disease spread. Never had FIP in your cattery? Then you are are
either FCoV negative, by design or good luck, or your cattery strain of
FCoV is a non-FIP causing FECV. There's enough evidence to indicate
that there are differing strains, the goodies and baddies, and Dr
Addie's household data showed that variation in a strain, as it was
replicated and transmitted within a household, was little. It's just
that as yet there's no way of knowing whether any strain will mutate
and cause FIP until it actually does. Should you do anything other than
practice good husbandry and not let numbers spiral?
a) Don't visit studs or have queens to visit without antibody testing
both parties. Obviously this is essential if you are maintaining a
negative cattery, but otherwise consider 1:400 or below as the guide.
Dr Lutz's study demonstrated that the higher the antibody titre, the
greater the viral load and viral shedding, and you certainly can't tell
a goodie from a baddie. (I'm 99.9% sure this is how I introduced my
virulent virus, though no cat belonging to either owner, or their
breeders, had cats with FIP as far as was known.) Even where there has
been no FIP, you don't want to swap viruses if you can prevent it, so
don't let the stud and queen share litter boxes. House them separately
if you possibly can.
b) Before introducing new cats into your cattery, titre test, and again
use the 1:400 as a guide. Isolate a newcomer for 3 weeks on arrival,
and certainly don't let let him/her mix with any kittens you have.
Sporadic Incidence of FIP, or wanting to reduce/eradicate FCoV? As
above. Also: a) Titre test all and isolate those with a high titre.
Test and re-test these at 6 weekly intervals. Consider most strongly
adoption to single cat homes for those that maintain a consistently
high titre over 3 testings. There are 2 reasons for this. These are
cats shedding great amounts of virus who are infecting and reinfecting
other cats in your household. In spite of care to separate out mothers
and kittens it is very difficult not to take virus from one part of a
cattery to another when there is a high viral load (difficult to
downright impossible according to the recent studies). Also these cats
that do carry and shed greater amounts of virus are probably the least
resistant to it. The aim should be to breed from cats that can cope
with it effectively. Those whose antibody levels drop to 0, or at least
below 1:400 are those who are dealing with it, and have the healthy
immune system you want to pass on to the next generation. b)Use early
weaning if you are happy to do this. It has been shown to be effective
in eliminating FCoV from kittens and they go to new homes seronegative.
If you're not comfortable with this because of stress to mother and
kittens, or have difficulty weaning them at an early age, then at least
keep each litter isolated with their mother away from all other cats in
the household. Keep separate litter boxes for queen and kittens, and
part them for periods so that mother uses her own, and ensure the
kittens have no access to it. c) Studies (Pedersen at Davis, J Norris,
who reported this year a disproportionately high incidence of FIP in
the Australian Mist population) have shown there is a genetic link.
Don't breed together cats that both have had kittens die of FIP.
Consider removing from the breeding programme a male that sires kittens
who succumb to FIP, with 2 or more females. (It's not that males carry
genetic predisposition any more than females. It's that by the number
of kittens they may produce they have a much greater genetic input to
future generations than females). d) As stress is a factor in FIP
developing, it's probably also useful to take into account the
temperament of breeding cats. e) Don't have a constant throughput of
cats in your cattery, buying in show and/or breeding stock frequently.
It causes stress and adds to chances of importing fresh viral strains.
Work with what you have. (That goes for all breeders not just those
With a FIP problem). I think that's just about covers it. I don't think
there's a lot that 's actually new, other than testing for, and
removing the high viral shedders, and recommendations of a titre score
to go below. I should just add that testing should be done by the
recommended Universities and Institutes rather than commercial labs.

Jen Lacey
Jenanca Korats at the Cottage Cattery