FIP Feline infectious peritonitis
 
 
 
Jacqueline Norris BVSc (Hons), MVSt, PhD, Grad Cert Educ (Higher) -Senior Lecturer in Veterinary Microbiology -- Faculty of Veterinary Science - University of Sydney - jnorris@mail.usyd.edu.au  


Extensive research efforts worldwide has led to a new understanding of Feline Coronavirus
(FCoV) infection and FIP but has produced an even greater number of questions that remain
unanswered. Currently there is no effective prevention or treatment for FIP. Equally, there is no
method of accurately predicting which cats are at risk of developing the disease. The
invariably fatal consequences, lack of predictable disease patterns, ineffective treatment
regimes and the significant emotional and financial impact of FIP makes it a formidable
disease.
Background 
FIP is a fatal immune mediated disease of 
wild and domesticated cats (Felidae) 
caused by mutant strains of Feline 
Coronavirus (FCoV). It is one of the most 
important causes of death in young cats. It 
occurs in cats of all ages but most 
commonly those under 3 years.  
 
The disease was first described in 1963 by 
Holzworth as a syndrome known as 
“chronic fibrinous peritonitis” but the 
name, along with the current name of FIP, 
is limiting in its description of this incredibly 
variable disease. FIP is now known to 
manifest as varying degrees of  
1) systemic serositis (inflammation of the 
serous membranes eg. the superficial 
surfaces of the abdominal or thoracic 
organs leading to wet FIP),  
2) vasculitis (inflammation of the blood 
vessels) and  
3) disseminated pyogranulomas (many 
areas of inflammation in body organs, 
consisting of the white blood cells called 
macrophages and neutrophils).  
 
The first reported appearance of FIP in 
Australia was in 19741, 2 but despite the 
anecdotal evidence of its frequent 
occurrence in Australia, there has been a 
conspicuous absence of peer-reviewed 
reports until a recently review of 42 cases.3  
 
Viruses within the family Coronaviridae, are 
known for their tendency to mutate 
frequently during viral replication 
(reproduction). Feline coronaviruses are 
typical in this regard.  The exact nature of 
the FIP inducing mutations are still 
unknown but are likely to be complex. The 
3C, 7B and spike genes are now 
considered to be most important in the 
development of FIP-causing mutant FCoV 
although the mutation occurs at various 
points along these genes. A key feature of 
the mutant FCoV is the ability to replicate 
in large numbers in a type of white blood 
cell known as the macrophage (also 
known as monocytes when circulating in 
the bloodstream). It is on this principle that 
the only reliable diagnostic tests for FIP are 
based.  
 
To complicate matters further, the role of 
the immune system in protecting against 
disease in some animals, while contributing 
to the disease in others, is another poorly 
defined issue in the development of FIP.  
 
Genetic susceptibility 
FIP is reported to occur more frequently in 
cats from catteries, boarding facilities and 
multicat households.4 While no breed 
predisposition has been firmly established, 
certain bloodlines and matings within a 
breed may be at greater risk.5 The 
incidence of FIP in purebred catteries 
increases in proportion to the number of 
animals kept in that facility. Environmental 
factors, however, are not the sole 
contributor to FIP susceptibility.  Foley and 
Pedersen (6) determined that FIP 
susceptibility was a partially heritable trait, 
with close relatives of affected cats within 
four Persian and one Birman catteries 
being significantly more likely to die of FIP 
than unrelated cats.  


 Figure 1: Inbreeding in cheetahs has led to an 
increased susceptibility to infectious diseases 
including feline infectious peritonitis. 

Of the non-domestic felids, cheetahs have 
been found to be especially susceptibility 
to FIP.  Inbreeding in this species has 
predisposed them to diseases involving a 
variety of infectious agents, including 
FCoV.7 Conversely, cats from some 
Abyssinian bloodlines have been reported 
to have significantly longer survival times 
after experimental challenge with virulent 
FIP strains than other breeds, suggesting an 
inherited resistance to FIP.6, 8  
A retrospective study in Australia9 found 
that purebred cats were over represented 
in the FIP cohort while DSH were under 
represented.  Within the purebred cats, 
Burmese, Australian Mist, British Shorthair 
and Cornish Rex cats were significantly 
over-represented, while Persian cats were 
under-represented, dispelling the 
explanation of husbandry practices being 
the only contributor to the incidence of 
FIP.  The overrepresentation of certain 
purebreds, most notably the Burmese and 
BSH cats has been mirrored in the 
demographics of confirmed cases of FIP 
received via clinical samples (tissues and 
effusions) submitted to our diagnostic lab 
over the past 3 years from all over Australia 
(Veterinary Diagnostic Pathology Services, 
The University of Sydney).  In our 
observations, other breeds or at least 
breed lines have also been noted as 
‘breeds of interest’ due to an increase 
number of cases of FIP. These breeds 
include the Birman and Ragdoll. 
Conversely we now rarely see cases of FIP 
in Australian Mists. Our research team is 
currently investigating the differences in 
the immune response between different 
breeds of cattery-confined cats to gain an 
understanding of factors that make some 
cats more susceptible to FCoV infection 
and the disease FIP.  
While FCoV antibody titres are unable to 
predict which cats will go on to develop 
FIP, it is widely accepted that the 
magnitude of the FCoV antibody titre 
broadly reflects the viral load within a 
given cat.10, 11 In other words, a cat with a 
high antibody titre to FCoV will have a 
high FCoV load in its body and is likely to 
be shedding virus in the faeces. Although 
this is not a direct predictive relationship, 
some researchers have speculated that 
certain cats with persistent and/or high 
FCoV antibody titres, given the right host 
(cat) susceptibility, are at a greater risk of 
developing FIP due to the greater risk of 
viral mutations occurring.12, 13  The exact 
titre that constitutes a ‘high’ titre varies 
markedly depending on the test used. 
Kummrow and colleagues suggested the 
guideline listed in the table below.14  
 
Recent studies in Australia15-17 have further 
highlighted a possible role of genetics in 
the development of this immune 
mediated viral disease. In serum antibody 
surveys conducted in household and 
cattery confined cats it was found that 
certain cat breeds had significantly higher 
antibody titres than other breeds.17 In an 
Australia wide retrospective study of 637 
cats,16 the FCoV antibody titres of Siamese, 
Persians, DSH and Bengal cats were 
significantly lower than that of British 
Shorthair, Cornish Rex and Burmese cats.  
In a Sydney based serum antibody study of 
household pet cats,17 the antibody titres of 
DSH, Persian, Siamese and Devon Rex cats 
were significantly lower than that of 
Burmese, BSH, Abyssinian, Birman, Ragdoll, 
and Russian Blue. The significant 
relationship between the breed of the cat 
and the FCoV antibody titre, especially in 
those breeds identified to be at greater risk 
of developing FIP, further supports the 
notion that breed (genetic) related 
differences exist in the immunological 
response to FCoV infection.  
 
Considerable work into the differing 
immune responses to FCoV and the role of 
genetics in controlling these immune 
responses is required if we are to have any 
chance of controlling this disease.  


Transmission 
FCoV infection is common in cattery- 
confined cats (80-100%) and pet cats (20- 
35%) worldwide due to faeco-oral 
transmission and environmental resistance 
of the virus. While it is endemic in many cat 
populations, the outcomes of infection are 
variable. Understanding the modes of 
transmission of Feline Coronaviruses 
requires knowledge of the virus location 
and its ability to infect tissues within the 
body.  
 
FCoV is a fairly fragile virus that is 
destroyed by most household disinfectants 
and detergents. It can however survive up 
to 7 weeks in dry conditions eg dried 
faeces, carpet etc. The most common 
method of FCoV transmission is via virus- 
infected faeces, although in the first few 
hours to days of infection it can be shed in 
the saliva and respiratory droplets. Usually 
kittens are infected with FCoV from their 
mother or other FCoV excreting cats, at 
the age of 6 to 8 weeks, when their 
maternal antibodies wane. Maternal 
antibodies are thought to protect kittens 
from FCoV infection until this time, as most 
kittens that are removed from an 
environment of FCoV shedding cats at 5 to 
6 weeks do not become infected.(10) 
  
Figure 2: Faeco-oral transmission of feline 
coronaviruses is facilitated by the use of communal 
litter trays. 
 
Replication of the feline coronaviruses in 
clinically normal cats occurs mainly in the 
intestinal lining (enterocytes). However 
these viruses are known to infect 
monocytic cells, circulate in the blood and 
spread systemically even in clinically 
normal cats,18, 19 although their ability to 

Shedding of infected enterocytes from the 
intestinal villi means that virus is shed in the 
faeces and cycles through the feline 
household via faeco-oral route. Testament 
to this is the finding in Australia (and many 
other parts of the world) that 98% of cats 
within catteries are infected with FCoV, 
and only 34% of pet cats are infected, with 
cats in single cat households significantly 
less likely to be infected.15, 17 The interesting 
finding in our studies has been the 
variation in antibody titres and likely viral 
loads between cats in the same cattery 
environment.  For example, in one cattery 
the antibody titres ranged from 1:400 to 
1:25,600 and this variation was not related 
to the age of the cat. 
 
Many apparently healthy cats who are 
persistently infected with FCoV play an 
important role in recycling FCoV in 
multicat environments. FCoV shedding 
cats produce many millions/billions of virus 
particles in their faeces, some of which 
can be spread to the environment during 
digging of litter (Figure 2).   
 
There is considerable debate over how a 
persistently FCoV infected cat develops 
FIP. One theory is that a mutation of the 
virus occurs within an individual cat. The 
formation of mutant strains is thought to 
confer the ability to infect large numbers 
of macrophages and reproduce large 
volumes of the virus. This theory is 
substantiated by recent work of Kipar and 
colleagues20 which showed (using real 
time RT-PCR) that cats with FIP have 
considerably larger viral loads in the areas 
of the body that produce blood cells (eg 
spleen, lymph nodes) than healthy FCoV 
infected cats.  These mutant forms of FCoV 
are thought NOT to shed faecally but are 
contained within the internal structures of 
an infected animal. Greater than 40% of 
cats with FIP will shed the enteric based 
FCoV, however the mutant forms of the 
virus (previously called FIPV) has not been 
found in the secretions or faeces from cats 
with FIP to date. Therefore transmission of 
mutated FCoV from one cat to the next is 
considered unlikely under natural 
conditions. It is theoretically possible, 
although not substantiated by current 
research, that cats with FIP lesions in the
kidneys or intestines may shed virus. This 
theory has been put forward to explain 
some reported “outbreaks” of FIP. 
Alternatively, the existence of 
immunocompetent carriers of the mutant 
virulent form of FCoV may explain these 
infrequent occurrences. Neither of these 
theories have been substantiated. When 
dealing with FIP within litters of kittens it is 
important to also consider the role of cat’s 
susceptibility in the development of 
disease as frequently only certain kittens 
within a litter are affected. It is important 
NOT to condemn litter mates of kittens 
affected by FIP. We have many examples 
of litter mates who have lived long healthy 
lives despite the demise of their litter mate 
and in many cases while cohabitating with 
the affected kittens. 
 
One final important point about 
transmission is that veterinarians when 
dealing with the effusions of cats with wet 
FIP or performing post-mortems within the 
clinic should be aware that these fluids 
and tissues are highly contagious to other 
cats and pose a significant threat for the 
subsequent development of FIP if hospital 
cats are exposed to the virus. 
 
 
Development of Disease 
The development of FIP is still a poorly 
understood disease process. Most of the 
pathology seen is caused by the cat’s 
immune response to the virus. Two theories 
have been proposed to explain 
subsequent events. One theory is that 
mutant FCoV infected macrophages exit 
the blood vessels and enter the tissue. The 
virus attracts antibodies and certain 
proteins known as complement. More 
macrophages and neutrophils (two types 
of white blood cells) are attracted to the 
tissue, leading to the development of 
pyogranulomatous lesions. An alternative 
theory suggests that circulating immune 
complexes deposit on the blood vessel 
walls, leading to the release of substances 
that cause the lining of the blood vessels 
to leak fluid. This allows FCoV infected 
monocytes to enter the tissue. Release of 
further substances from infected and dying 
monocytes stimulates further blood vessel 
leakage and the development of high 
protein fluids into the abdominal/chest 
cavities in some cases. The immune 
mediated vasculitis and the formation of 
pyogranulomas are the key features of FIP 
seen in microscopic sections.  
 
 
Figure 3: This section of liver has been stained using the 
specialised technique known as immunohistochemistry. On the outside of the picture are normal liver cells, while the concentration of cells in the centre shows a typical 
pyogranuloma . The brown staining cells are FCoV infected 
macrophages.  
 
 
Clinical Presentation 
The clinical presentations of FIP are 
variable and often complex, reflecting 
variations in the virus itself, the nature of 
the cat’s immune response and the 
influence of environmental stresses.  
Approximately 50% of all cats diagnosed 
worldwide are less than two years old and 
purebred cats are generally over 
represented. Two broad forms of the 
disease have been described across all 
ages and breeds: “effusive” (wet) or “non- 
effusive” (dry).  Despite this apparent 
division, these are not distinct disease 
entities. Cats with non-effusive FIP may 
develop effusions in the terminal stages of 
disease and conversely, there are reports 
of non-effusive FIP being preceded by a 
subtle effusive form of the disease.  
 
Typically, patients with effusive FIP have 
high protein abdominal, pericardial 
(around heart) and/or thoracic (chest) 
effusion(s), fever, weight loss, anaemia 
and elevated serum globulin levels, 
although not all cats adhere to this 
stereotype.  The non-effusive form of FIP is 
often more vague in its presentation with 
non-specific signs including fever, weight 
loss, and inappetance.  Clinical signs, 
beyond the non-specific, relate to the  
tissues affected.  Possibilities include liver, 
kidney, pancreas, spleen, abdominal 
lymph nodes, central nervous system 
(CNS), gastrointestinal tract (GIT), eyes, skin 
and heart. Usually more than one body 
system is involved but occasionally only 
one is affected e.g. CNS or GIT, and 
clinical signs are restricted to this particular 
system.  
 
Studies in Australia (9) compared the clinical 
presentations of FIP in Australia’s 
geographically isolated cat population 
with overseas reports. Significant features 
of this study were i) the over-representation 
of certain breeds (Burmese, Australian Mist, 
British Shorthair, and Cornish Rex) and the 
under-representation of other breeds 
(Domestic Shorthair, Persian); ii) the 
overrepresentation of males (2 to 1); iii) the 
even age distribution of disease seen in 
cats older than 2 years-of-age; and iv) the 
presence of immune-mediated 
haemolytic anaemia (red blood cell 
destruction) in two cats in that study plus 
three cats subsequent to the study.  
 

Figure 4: The age distribution of cats presented with 
feline infectious peritonitis in the study by Norris et al 
2005. 
 
Diagnosis 
The difficulties in diagnosing FIP have been 
a hot topic in feline medicine for many 
years. Adopting traditional instruments of 
infectious disease diagnosis (eg PCR, 
serology) for FIP diagnosis and FCoV 
infection control has led to ongoing 
confusion for vets and unwarranted 
euthanasia of cats. This has stemmed from 
an incomplete understanding of the 
dynamics of FCoV infection in cats and 
the development of FIP. Diagnostic tests 
for FIP must therefore rely on the biological 
behaviour of the virus. A key feature of the 
nasty mutant FCoV is the ability to 
reproduce in large numbers in 
macrophages and monocytes and it is on 
this premise that the only reliable 
diagnostic tests for FIP are based.  
 
The clinical similarity between FIP and 
many other feline diseases, coupled with 
the non-specific nature of many of the 
tests available, makes the definitive 
diagnosis of FIP difficult even when the 
diagnostic approach is broad and 
thorough. While a cat presented with 
elevated blood globulin (type of protein), 
fever, and high protein abdominal and/or 
thoracic effusion may be highly suggestive 
of FIP, the variation in clinical 
manifestations beyond this stereotype is 
remarkable.  
 
The advent of FCoV antibody titres and RT- 
PCR (reverse transcription polymerase 
chain reaction) has added to the 
complexity due to the indistinct 
differentiation between mutant FIP- 
causing FCoV and those FCoV that are 
unlikely to cause disease.  While these tests 
were first met with enthusiasm, it is now 
known that it is not possible to differentiate 
between the harmless and mutant forms of 
the virus by RT-PCR or any FCoV antibody 
test to date. This severely limits their use in 
the diagnosis of FIP. Of greater concern is 
the finding by several researches of FCoV 
infection in the tissues of healthy cats 
without clinical signs, highlighting the need 
to exercise care to avoid over 
interpretation.  In other words, performing 
RT-PCR, a technique that detects tiny 
amounts of virus in tissue or blood cannot 
be used for the diagnosis of FIP as many 
normal cats have small amounts of FCoV 
at these sites. Recent developments in the 
detection of replicating FCoV within 
circulating monocytes by RT-PCR however 
look more promising.21 This is now available 
in the USA but must be interpreted with 
great caution and should not be used in 
isolation.  
 
Despite these limitations, FCoV antibody 
titres are still used indiscriminately for the 
diagnosis of FIP. A clinician must carefully 
consider the environment and age of the 
cat in question. For example a high 
antibody titre from a young cat or a cat 
from a multicat household is impossible to 
interpret and is in no way helpful for the 
diagnosis of FIP. Incorrect interpretation 
can lead to incorrect diagnosis and 
unnecessary euthanasia. To use the words 
of Neils Pederen, an eminent researcher in 
FIP, “more cats have died from the 
misdiagnosis of FIP than from FIP itself”. 
 
The detection of characteristic 
microscopic changes within affected 
tissue (biopsy or post mortem) has been 
considered the only conclusive test for FIP 
for a considerable time and detecting 
virus within macrophages in the areas of 
pathology using immunohistochemistry 
allows definitive confirmation of the 
diagnosis.  In a disease process where the 
treatment of choice is often euthanasia, 
diagnostic accuracy is essential. 
 
a) Serum biochemistry and haematology 
The results of routine blood tests 
(biochemistry and red and white blood 
cell counts = haematology) found in 
association with FIP are non-specific and 
non-diagnostic. They may include 
elevated serum protein due to elevated 
globulin, increase bilirubin (may appear as 
jaundice clinically), anaemia, and white 
blood cell changes traditionally seen with 
stress.  These are found in many other 
diseases.  In addition, blood tests specific 
to affected organs (eg kidney, liver) MAY 
be elevated. Hartman and colleagues22 
compared the value of certain diagnostic 
tests in the largest study of FIP cases to 
date and found that elevations of total 
serum proteins above 80g/L was only 60% 
specific for FIP.  This highlights the need to 
view elevated serum protein as being 
supportive of a diagnosis of FIP and several 
other diseases, but of limited diagnostic 
value when in the normal range.  In cases 
in which total serum protein is elevated, 
additional supportive evidence for FIP can 
be gleaned from measurement of 
albumin-globulin ratios, γ-globulin 
concentrations and α1-acid glycoprotein. 
None of these tests are conclusive and are 
considered merely supportive or 
circumstantial evidence (not enough to 
convict a cat of FIP).  
While blood profiles can provide essential 
baseline information in the investigation of 
sick cats, clinicians cannot exclude 
disease in certain body organs simply due 
to the absence of abnormal findings.  In 
our retrospective study of cases, some cats 
with extensive pathology in the kidney or 
liver had normal serum biochemical test 
results. 
 
b) Measuring FCoV antibody titres 
The difficulties in interpreting antibody titres 
of FCoV have led to widespread 
acceptance that diagnosis of FIP by 
antibody titres is neither possible nor 
appropriate. Despite this, antibody titres 
continue to be given undue emphasis in 
the diagnosis of FIP. The antibody titre to 
FCoV in cats with FIP varies according to 
the nature of the clinical syndrome. There 
is considerable variation in the reported 
magnitude of anti-FCoV antibody titres in 
cats with confirmed FIP, with considerable 
overlap with healthy patients, making 
interpretation difficult. Indeed, a negative 
antibody titre alone cannot rule out a 
diagnosis of FIP, while a high FCoV 
antibody titre certainly does NOT confirm a 
diagnosis of FIP.  The emergence of tests 
that claimed to measure antibodies 
against mutant FCoV alone became 
popular but their validity was NEVER 
supported by peer reviewed publications 
and they are now considered of no 
greater value than other antibody tests.  
The gold standard for measuring antibody 
levels to FCoV is by indirect 
immunofluorescence (IFA), a test that is 
now available in several diagnostic 
laboratories in Australia. Hartmann22 has 
reported that cats with antibody titres of 
1:1600 had a very high probability (94%) of 
having FIP, however it is noteworthy that 
this study compared cats with FIP to sick 
cats with diseases clinically similar to FIP. 
Healthy cats from multicat environments 
were not included in that study and the 
authors of that paper comment that a 
high titre from a cat in a multicat 
environment is not predictive of FIP due to 
the high level of FCoV in those 
environments.23 In addition, the method 
used in that paper is different to those 
used in Australia. Currently all labs in 
Australia use a method of indirect 
immunofluorescence that involves feline 
cells infected with a FCoV (type not 
always specified). Studies in Switzerland by 
Kummrow and colleagues14 have shown 
that measuring the antibody titre using 
different cell lines and coronavirus types 
produces markedly different antibody 
levels.   
In our studies at the Faculty of Veterinary 
Science, University of Sydney (manuscript 
in preparation), we measured the FCoV 
type 1 antibody titres in 306 clinically 
healthy cattery confined breeding cats 
throughout NSW. Their antibody titres 
ranged from zero to 1:102,400. Over two- 
thirds of cats (213/306) had FCoV type 1 
antibody titres of 1:1600 to 1:6400. This is 
shocking to most cattery owners who are 
used to the antibody titres reported by 
Addie and colleagues that have an end 
titre of 1:1280 and use FCoV type 2 
infected cells in their indirect IFA method. If 
cats are infected with FCoV type 1 and the 
titre is measured with FCoV type 1 infected 
cells, the titres reached may be 
considerably higher than if measured 
using another coronavirus.  
While there is a very important role for 
antibody titres in the management of 
multicat households and the identification 
of shedders, its use in the diagnosis of FIP in 
individual cats is a dangerous exercise.  
They can never be used alone to 
determine a cat’s fate.  
 
c) Fluid analysis and direct 
immunofluorescence  
The analysis of thoracic and abdominal 
fluid is an essential diagnostic test in 
effusive FIP. Microscopically, FIP effusion 
typically consists of low numbers of 
neutrophils and mononuclear cells 
(macrophages). The presence of a high 
protein effusion and low to moderate 
number of cells as described above is 
helpful in providing further evidence for 
the likelihood of FIP, but has been found in 
other disease processes.   
Albumin/globulin ratios in serum and 
effusion can be useful in the diagnosis of 
FIP but are not specific for FIP, so must be 
interpreted in light of all other evidence. 
Serum albumin/globulin ratio <0.8 has a 
high probability (92%) of FIP while an 
effusion albumin/globulin ratio <0.4 also 
has a high probability of FIP. 
 
Techniques have been devised to detect 
the presence of FCoV in macrophages 
within the effusion. The method most 
commonly used worldwide is direct 
immunofluoresence. This technique uses a 
fluorescein labelled anti-FCoV antibody to 
detect large amounts of FCoV within 
macrophages, an important differentiating 
factor between FCoV based in the 
intestines and mutant forms of FCoV. 
Hartmann and colleagues found that 
direct immunofluoresence was extremely 
reliable at diagnosing FIP when positive 
but can be unreliable when negative due 
to the high rate of false negatives.22  
Immunofluorescence is best done after 
fluid analysis. In Australia it is available at 
the Veterinary Diagnostic Pathology 
Service (The University of Sydney) and 
VETPATH® a private commercial lab in 
Perth. The test relies on the macrophages 
within the fluid being in good shape, so 
delays in sampling lead to leakage of 
FCoV from the macrophages and 
increases the probability of a false 
negative result. Tests are run daily in our 
laboratory, with results available on the 
same day the sample arrives to our 
laboratory.   
 
 
Figure 5: Direct immunofluorescence uses a 
fluorescein labelled anti FCoV antibody to detect 
large amounts of FCoV within macrophages 
 
d) Histopathology + immunohistochemistry 
The detection of characteristic 
microscopic changes from biopsy samples 
has been considered the only conclusive 
test for FIP for a considerable time. Not all 
cases of FIP have classical microscopic 
appearance and this has led to the 
development of more sensitive and 
definitive diagnostic tests such as 
immunohistochemistry.  
 
Immunohistochemistry (IHC) is a sensitive 
and specific technique used in many 
infectious and neoplastic (cancer) 
diseases. In the diagnosis of FIP we use an 
antibody against FCoV to detect virus 
within macrophages in formalin fixed tissue 
sections (biopsy samples). It is used 
subsequent to histopathology to 
definitively confirm FIP in those cases when 
the microscopic findings are inconclusive 
or in some cases when the diagnosis must 
be confirmed conclusively (eg for cat 
breeders due to the implications in 
breeding).  This technique only detects 
macrophages with sufficiently high 
numbers of FCoV and allows the 
macrophage to be view in context with 
the surrounding pathology.  Our laboratory 
is currently the only one in Australia 
offering this diagnostic test. All the external 
laboratories in Australia routinely send 
sections of the tissue to our laboratory for 
testing and therefore can be requested on 
any tissue sample through your usual 
veterinary pathology service.  
 
 
Management of FCoV and FIP in 
breeding catteries 
Confirming FIP as the definitive diagnosis 
using histopathology +/- 
immunohistochemistry is the essential first 
step. Once FIP is confirmed, an analysis of 
the breedline is required. Mapping the 
pedigree of the affected cat and noting 
any confirmed cases of FIP along the 
family tree can be helpful. In several cases 
it has been possible to identify a common 
stud or queen that should be desexed and 
removed from the breeding program.  
Determining the Feline Coronavirus load of 
individuals within the cattery is a useful 
exercise if the information is used correctly. 
Using RT-PCR to identify FCoV in the faeces 
of cats, Diane Addie and colleagues in the 
UK have determined that there are four 
possible outcomes of exposure to FCoV 
infection (www.dr-addie.com): 
“1. The kitten or cat develops FIP (around 
5- 10% of infections). 
2. The vast majority of cats shed FCoV for a 
while, develop antibodies, stop shedding 
FCoV and their antibody titre returns to 
zero. 58% of FCoV shedding lasts up to one 
month and 95% of virus shedding lasts less 
than 9 months. 
3. The cat becomes a lifelong FCoV carrier 
(13% of infected cats).  These cats shed 
FCoV continually in their faeces and most 
remain perfectly healthy although some 
develop chronic diarrhoea. 
4. Resistant cats – around 4% of cats 
appear to be completely resistant to FCoV 
infection, they don’t shed the virus and 
they mount an almost undetectable 
antibody response. “ 
 
Their work24 also determined that a single 
faecal RT-PCR result on its own is 
meaningless because some cats may be 
intermittent shedders of FCoV. RT-PCR 
testing has to be part of a series of tests 
and is best accompanied by 
immunofluorescent antibody (IFA) testing 
because RT-PCR can be prone to both 
false positive results and false negative 
results. Delays in getting the faeces sample 
to the laboratory and at the incorrect 
temperature causes destruction of the viral 
RNA, leading to a false negative.  
 
Establishing that a cat has eliminated 
FCoV infection requires five consecutive 
negative monthly RT-PCR results on faeces 
OR a reduction in the FCoV antibody titre 
(by indirect IFA) to less than 1:10. This may 
take months to years to achieve in some 
cases. These combined methods can be 
useful in determining life long shedders of 
FCoV. Removal of these cats from multicat 
environments such as catteries is essential 
for control of FCoV.  
 
In Australia, RT-PCR is not currently 
available however measurement of serum 
antibody titres to FCoV using indirect IFA 
can provide some helpful information. It is 
accepted that the magnitude of the FCoV 
antibody titre broadly reflects the viral load 
within a given host.10, 11 Monitoring of these 
values over time (every 6 to 12 months) 
can provide information to the breeder 
and veterinarian as to which cats are 
chronic shedders and when the results are 
examined for the whole cattery they can 
be an indication of the success or failure of 
husbandry changes. When measured 
using indirect IFA with type 2 FCoV (Addie 
et al), cats with low titres (1:25 or below) 
are not shedding FCoV in their faeces. 
Cats with high titres (1:400) are almost 
always shedding high levels of virus. (NB In 
Australia, FCoV type 1 testing is performed 
and these give much higher readings, not 
comparable with the above). Some of 
these cats will stop shedding upon isolation 
in a single cat household (detected by a 
decrease in their titre). If the cat is 
persistently shedding virus the titre will 
remain high. Some catteries have attained 
FCoV free catteries using these methods. 
Screening for FCoV in any cat entering this 
cattery is essential if the FCoV free status is 
to be maintained. 
 
Analysis of the husbandry practices of the 
cattery (cleaning and number of litter 
trays, use of disinfectants, cleaning and 
management of food bowls etc) in the 
cattery can lead to some helpful changes 
in cattery management, which will assist in 
reducing the faeco-oral cycling of enteric 
based FCoV between cats. While it might 
seem obvious to many, ensuring the food 
bowls and litter trays are not cleaned in 
the same area or with the same cleaning 
instruments is essential. This has been an 
issue in several catteries and rescue 
agencies.  
 
Recent studies by Addie and colleagues in 
UK (unpublished; www.dr-addie.com) 
have found that there is considerable 
variation in the virus killing ability of kitty 
litters. All the UK brands of kitty litter made 
of Fuller’s earth were found to be much 
more effective at killing FCoV than other 
types, although these clumping litters have 
risks associated with oral ingestion in 
kittens. Further research in this area would 
be useful. Using dedicated litter trays for 
each cat or cat group, removing faeces 
from litter trays as often as possible (1-2 x 
daily) and using dedicated poop scoops 
for each cat pen or tray is also 
recommended.  
 
 
Figure 6: Ensuring that food bowls and litter trays are 
not cleaned in the same area is essential 
 
Addie and Jarret have successfully 
implemented early weaning protocols for 
the prevention of FCoV infection in kittens 
born in FCoV endemic catteries. This 
involves isolating the queens 2 to 3 weeks 
before parturition, strict quarantine of the 
queen and her kittens in a separate room 
from the rest of the cattery, and weaning 
at 4 to 6 weeks of age. This protocol is 
based on the finding that kittens are 
protected from FCoV infection by their 
maternal antibodies until 5-6 weeks of age, 
when the maternal antibody wanes. The 
maintenance of an isolated quarantine 
area requires strict vigilance.  Some find it 
difficult to achieve and argue that the 
early weaning has a social cost on the 
kittens. Although a kitten may be 
successfully raised free of FCoV it may 
become infected later in life and therefore 
the purpose of isolation and early weaning 
is to delay the age at which FCoV 
infection occurs.  
 
Management of a cat in contact 
with an FIP affected housemate 
There is no current evidence to suggest 
that a cat with FIP sheds the mutant virus in 
his/her faeces. It is likely that the cats in the 
household have been exposed to the 
same enteric based FCoV depending on 
their toileting habits in the household (ie 
cats that defecate outside are thought to 
be at lower risk of receiving the enteric 
form of FCoV from their housemates). 
Clients however will commonly present a 
housemate of an FIP affected cat for 
examination to determine its prognosis. It is 
likely that this in-contact cat may have an 
antibody titre to FCoV but this is in no way 
predictive of its fate. If a high FCoV titre is 
found the cat should be tested in 6 to12 
months. Most cats in single or two cat 
households will usually clear FCoV over a 
few months to years. A persistently high 
antibody titre does not necessarily indicate 
a poor prognosis. Conversely, a 
consistently low or negative titre is 
indicative that the cat is highly unlikely to 
develop FIP. 
  
Treatment options 
No therapies have been proved to
effectively treat FIP. Many 
immunosuppressive (prednisolone, 
cyclophosphamide, chlorambucil, 
thalidomide) or immunomodulating drugs 
(pentoxifylline) have been tried with 
several providing temporary and often 
short-term improvement.  
 
One immunomodulating drug, feline 
 recombinant interferon omega (Virbagen 
Omega®) has produced some 
encouraging results25 when used with 
prednisolone. The researchers used 
1MU/kg s/c eod in combination with 
glucocorticoid (prednisolone at 1mg/kg 
bid or dexamethasone), to treat 12 cases 
of FIP. Of the 12 cases, 4 cats were still 
alive and well after 2 years, 4 cats survived 
2 to 5 months while 4 cats survived less 
than a month. Eleven of the 12 cats had 
effusive disease. The age of the 4 cats who 
were in remission at 2 years, ranged from 6 
to 16 years and therefore were older. While 
criticism of the criteria for FIP diagnosis has 
been suggested by some, it remains the 
only drug protocol with the potential to 
limit the immune mediated tissue damage 
and limit viral replication. The exact 
mechanism by which this drug effects 
changes in the cat’s immune response is 
not understood at this time.

Use of this drug combination so far in our
hands has not met with overwhelming 
success. We have had marked 
improvement in clinical signs in two cats 
(of 15) with confirmed FIP. Both have been 
less than 3 years of age with pleural 
effusion. One cat (a 9 month old Burmese 
female desexed with effusive FIP (pleural 
fluid)) had a noticeable response to 
treatment with considerable reduction in 
pleural fluid and clinical control of the 
disease for 9 months before she had to be 
euthanased due to deterioration of the 
quality of life.  The second cat (2.5 year old 
male neutered Scottish Fold) with 
noticeably improvement in clinical signs 
and is currently going well (6 months since 
diagnosis). 
 
Katrin Hartmann and colleagues in  
Germany have recently completed a 
placebo controlled double blind clinical 
trial. In this study to soon be published (late 
2007 or early 2008), 37 cats with FIP were 
treated randomly with feline interferon-ω 
(106 IU/kg s.c. every 48 hours 7 days, 
subsequently once every week) or 
placebo. In all cats, FIP was confirmed by 
histology or immunostaining of FCoV 
antigen in effusion/tissue macrophages. All 
cats received glucocorticoids, either as 
dexamethasone (in case of effusion) or 
prednisolone. They found that there was 
no statistically significant difference in the 
survival time of cats treated with 
interferon-ω versus placebo. Cats survived 
for a period of 3 to 200 days (mean 18 
days). There was only one long-term 
survivor (> 3 months) that appeared to be 
in the interferon-ω group. This cat had 
been presented with effusion that totally 
disappeared; it did not show signs until 
euthanized 200 days after treatment 
initiation due to recurrence of FIP. 
Although there was no difference in the 
mean survival time, few cats may benefit 
from treatment including interferon-ω. 
  
Considerably more research is required to  
understand the complex immune response 
to FCoV and the development of FIP. With 
this will come opportunities to develop 
effective treatments or, even more 
importantly, methods of preventing FIP.   
 
 
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Surgery. 2004;6(2):107-109. mailto:jnorris@mail.usyd.edu.auhttp://www.dr-addie.comhttp://www.dr-addie.comshapeimage_2_link_0shapeimage_2_link_1shapeimage_2_link_2
FELINE INFECTIOUS PERITONITIS (FIP): Update 2007
Monday, October 1, 2007