Niels C. Pedersen, DVM PhD, Distinguished Professor Emeritus, Center for Companion Animal Health, School of Veterinary Medicine, University of California, Davis

A laboratory called AnimalLabs© in Zagreb, Croatia is now offering a test that they claim will identify cats that carry a genetic resistance marker for FIP (, accessed October 7, 2015). The same test is being offered by Genimal Biotechnologies in France (, accessed October 29, 2015).   AnimalLabs©  provided two references, one to the research article that described this marker1and a second review article on FIP that I published in 2009.2  The first article can be openly accessed at:   A synopsis of my 2009 review article is available at:  I want to assure you that the inclusion of my review article does not constitute an endorsement of the test.  In fact, I believe that the research behind this test was flawed in several respects and should have been considered as preliminary at best. 

I would like to summarize the research done in the article by Hsieh and colleagues.1  The researchers reasoned that interferon-gamma was involved in protection against FIP, a reasonable assumption based on earlier research of others.  They sequenced the feline interferon-gamma gene (fIFNG) and identified differences between cats (i.e., genetic polymorphisms) at three different positions that they referred to as 401, 408, and 428B.  These polymorphisms involved a single nucleotide polymorphism (SNP) at each of these positons.  These SNPs were not in parts of the genes that encode the fIFNG protein (i.e., exons), but rather in regions flanking the exons (i.e., introns).  Intronic regions are known to contain both nonsense sequences and genetic elements that regulate the level of protein expression by a gene.  They then collected DNA from 66 healthy cats and 60 cats with FIP.   They found no relationship between SNP differences at positions +401 and +408, but it appeared that there was a relationship with disease status for a SNP at position +428B.  Quoting their work – “from all the SNP tested; only fIFNG + 428C/T was found to be significantly associated with the outcome of the infection. At position +428, there was a higher frequency of the CT genotype in asymptomatic control cats (19.5%) than in FIP cats (6.3%), and the data showed a significant correlation with disease resistance (p = 0.03) (Table 2).”   It is noteworthy that only cats that were CC or CT were present among the 66 healthy and 60 FIP cats; no cats that were TT were present in both populations.  A table listing pertinent findings is given below:


                              Healthy cats                       FIP cats

+428 SNPs           (% of cats)                           (% of cats)

CC                   66 (80.5)                               60 (93.8)              

CT                   16 (19.5)                               4 (6.3)

TT                   0 (0.0)                                   0 (0.0)


The authors concluded that the difference between 16 healthy cats with CT (19.5% of healthy cats) was significantly different than 4 FIP cats with CT (6.3% of FIP cats).  Using an Odds Ratio (OR) they calculated that the odds of CC cats having FIP were 3.6 times greater than cats having CT and concluded that T SNP was dominant to C.  However, there were two problems with this conclusion.  First, no cats in their study were TT and given the fact that 20 cats in both populations carried the T SNP (20/126=15.8%), the expectation would be that 9% (.158 x .158=.092), or 11 cats among the 126 cats would be TT.   This suggests that either TT is an embryonic lethal, or more likely that the study populations were not random representation of all cats.  Statistical comparisons are only valid when dealing with populations that are randomly selected and special care needs to be taken when the significance level is close to the minimum of P≤0.05 and the numbers of case and controls is small. The zero value for TT cats in the population also prevented an assessment of whether or not cats containing two copies of the “protective allele” also had significantly more resistance than cats that were CC.  One would expect that if T is dominant, and CT is protective, that TT would also be protective.  Knowledge of the incidence of cats that are TT at +428 is critical for application of the test, because the only way to breed for CT genotype, if it is the only genotype associated with FIP resistance, is to maintain CC cats in the population.  If it can be shown that TT cats show a similar degree of FIP resistance to CT cats, then it is theoretically possible to breed only for the T allele (CT and TT), assuming that the T allele is really related to resistance.  Therefore, the value of the test is dependent on the incidence of CC, CT and TT genotypes in the populations where it will be used.  It is likely that some breeds will be homozygous for the common allele C, and the test will therefore not apply to them.  Although unlikely, some breeds may have a high incidence of T, and again assuming that both CT and TT are protective, it may not be cost effective to test.  If the incidence of T is low, positive selection for T carries the risk of inbreeding (see discussion below).  The bottom line is that breeders should not pay for this test until they are given the information that is necessary to properly use it in their breeding programs.   

The authors had the greatest problem trying to explain the biologic relevance of the T SNP polymorphism.  Most meaningful genetic mutations are in exon (protein coding regions) and not in introns (non-protein coding regions).  In order to provide biological relevance, the authors needed to show that the mutation in the intron caused an increase in the production of fIFNG.  The normal way to do this would be to isolate the normal gene having the CC SNPs and the alternative gene with the CT SNPs and show that there was a difference in expression levels of fIFNG between the two genes in some sort of test tube (i.e., in-vitro) system. The simplest test would be to identify a large cohort of cats that are CC, CT, or TT and isolate their blood lymphocytes, stimulate them to produce IFNG, and then compare the levels of either specific RNA (by qRT-PCR) or actual protein by ELISA or other assay.  If their observations are correct, lymphocytes from cats that are CT or TT should express more fIFNG than cats that are CC.  Rather than do this complex experiment, the authors chose to merely measure the levels of fIFNG in the plasma of cats with FIP, reasoning that cats with FIP and the CT SNPs would have higher plasma levels of fIFNG than FIP cats with the CC SNPs.  They found that 12/12 FIP cats with the CC SNPs had very low levels of fIFNG, while all three FIP cats with the CT mutation had high levels.  The conclusion was that the CT mutation allowed for a higher expression of fIFNG. There were several serious problems with this conclusion.  First, it is paradoxical that one would conclude that the CT mutation conferred resistance to FIP, and that this resistance was associated with increased fIFNG expression, but then prove it by using plasma from CT cats that were suffering from FIP.  The second problem is that there were only three cats in the CT group and 12 in the CC groups, rendering any statistical comparison moot.  Finally, there is not good evidence that cats develop FIP because they are unable to produce sufficient levels of fIFNG.  Several studies on FIP have measured cytokine expression in cats with FIP.3 These studies were more apt to show increases in fIFNG in serum of cats with FIP and increased production by blood lymphocytes of cats with FIP upon stimulation.  In fact, the general conclusion is that IFNG is stimulated in cats with FIP rather than inhibited.  . 

Up to this point, I am assuming that there is some merit in this research and that further research is warranted.  The problem is making the huge leap from a somewhat tenuous research finding to application in the field.  There is already ample evidence that resistance to FIP cannot be attributed to a simple polymorphism in a single gene. Our attempts to find a single gene responsible for FIP resistance in both field studies with Birman cats4 and with random bred cats in our own experimental breeding program5 have failed to identify a single genetic marker for FIP resistance/susceptibility that we would deem significant.  In fact, the only genetic risk factor that we could identify for FIP resistance was inbreeding itself.6 Breeding resistant cats to resistant cats did not increase resistance in their offspring, but rather made them even more susceptible.  This is exactly what you would expect from a genetic trait that involves many different genes and gene pathways.  The more you try to select for a single resistance factor, the more you unintentionally limit the role of multiple genes and gene pathways.  Interestingly, the current recommendation is still the best one, i.e., to avoid inbreeding and not to breed cats that have produced FIP kittens. This recommendation is based on the theory that such cats carry a greater proportion of susceptibility factors than cats that do not produce kittens that develop FIP and when bred together will produce kittens with an even greater proportion of risk factors.  Based on these findings, selecting for FIP resistance using a single genetic marker is more likely to favor inbreeding and actually increase the incidence of FIP.  Finally, it must be remembered that heritability only explains 50% of FIP susceptibility, 7 with the remainder being attributed to epigenetic (genetic changes occurring after birth) and environmental factors.  

Although a simple genetic test that will significantly reduce the risk of FIP does not seem likely, there is nonetheless reason to continue to search for genetic explanations for why some cats appear to resist FIP virus infection and others succumb to it, and why some cats develop the wet form of FIP and others the more chronic dry form.  These studies should be concentrated in catteries, where FIP exists, pedigrees are known and genetic traits can easily be tracked.  However, the cost for such research should not be born at the expense of breeders ordering a test. The normal sequence for the marketing of a genetic test for a disease trait is to validate it before offering it to the public.  I do not believe that this test has been adequately researched.  

References cited

1. Hsieh LE, Chueh LL. Identification and genotyping of feline infectious peritonitis-associated single nucleotide polymorphisms in the feline interferon-γ gene. Vet Res. 2014, 45:57.

2.  Pedersen NC. A review of feline infectious peritonitis virus infection: 1963-2008. J Feline Med Surg. 2009, 11(4):225-58.

3. Pedersen NC. An update on feline infectious peritonitis: virology and immunopathogenesis. Vet J. 2014, 201(2):123-32

4. Golovko L, Lyons LA, Liu H, Sørensen A, Wehnert S, Pedersen NC. Genetic susceptibility to feline infectious peritonitis in Birman cats. Virus Res. 2013, 175(1):58-63.

5. Pedersen NC, Liu H, Gandolfi B, Lyons LA. The influence of age and genetics onnatural resistance to experimentally induced feline infectious peritonitis. Vet Immunol Immunopathol. 2014, 162(1-2):33-40.

6. Pedersen NC, et al. Immunity to feline infectious peritonitis virus infection is diminished rather than enhanced by positive selection for a resistant phenotype over three generations.Manuscript in preparation.

7. Foley JE, Pedersen NC: Inheritance of susceptibility of feline infectious peritonitis in purebred catteries.  Feline Practice, 1996, 24(1):14-22.

The following is an article written by breeder and epidemiologist Cris Bird, Dr. P.H. She has a doctoral degree in public health from UCLA and is also an Old Style (Thais) Siamese breeder at Sarsenstone Cattery.  She shares her excellent article “A Word About FIP” with SOCK FIP.

A Word About FIP by Cris Bird, Dr. P.H.

One of us at Sarsenstone is an epidemiologist, a researcher who specializes in disease prevention and control, so we can’t resist talking a little about how to prevent and control feline infectious peritonitis, FIP.  We also encourage you to ask your veterinarian any questions you may have about FIP.

When you look at cattery ads and websites, you often see “We guarantee our kittens free of feline leukemia and FIV.”  Sometimes you see guarantees that kittens are free of ringworm and FIP, as well.  It is reasonable for a breeder to claim that her kittens are free of feline leukemia and FIV.  There are good screening tests for those diseases.  The tests are not perfect.  No test is.  But they are very, very good, about as good as screening tests can get.  If a breeder tests all new cats for feline leukemia and FIV and does not allow the new cats to join her other cats until she is sure they are negative for those diseases, and if she never allows her cats to wander outdoors, she can be confident, and so can you, that her kittens are leukemia and FIV-free.


Niels C. Pedersen,DVM, PhD; Director Center for Companion Animal Health, University of California, Davis, CA

Over 100 published articles have appeared in the world’s literature concerning FIP since my extensive review of FIP in 2009 (1). The following is a summary of significant findings from a portion of these published works.

Origin of FIPV (the FECV to FIPV mutation)

The debate over the origins of the FIP virus (FIPV) continues to some degree, but there is no doubt that FIPV arises as a mutant of the ubiquitous feline enteric coronavirus (FECV). Although FIPVs are virtually identical genetically to FECVs within the same environment (2-4), FIP causing mutations are nonetheless unique to each cat (2,3,5,16). The nature of the mutations that cause an FECV to change to an FIPV has been the topic of several recent publications. The 3c accessory gene mutations were the first to be implicated in FECV-to-FIPV conversion (reviewed 1) and these findings have been corroborated by additional studies (2,3). However, a group from the University of Utrecht, after sequencing the complete genomes of a large number of FIPVs and FECVs, found a second mutation that occurred only in FIPVs (5). This mutation consisted of one or more single nucleotide polymorphisms (SNPs) in the fusion domain of the spike (S) gene that caused minor (synonymous) changes in single amino acids within this region.


The following text originated in an interview with Dr. Niels C. Pedersen by Nancy Reeves , published in October 2008.


FIP is caused by a feline coronavirus.Coronaviruses of various species exist in most types of animals and humans and usually cause acute respiratory or enteric disease.FIP is the cause of death of 1 in 100 to 1 in 300 cats in U.S.The incidence can be 5 or more times greater among young cats coming from catteries and shelters and is the major cause of abdominal fluid (ascites) and intraocular and neurologic inflammatory disease in cats under 3-5 years of age.FIP is virtually 100% fatal and there is no good prevention.The emotional toll of FIP is especially great, because it strikes suddenly weeks, months and even years after initial infection.Therefore, cat lovers usually experience this disease long after they have developed strong emotional bonds with their new pet.


Coronviruses are ubiquitous among all cat populations and the principle one of cats is correctly referred to as feline enteric coronavirus (FECV).FECV is present in virtually all catteries with 6-8 or more cats and up to 40% or so of the kittens relinquished to shelters. The enteric virus in the cat population lives in the digestive tract and is shed in feces. Cats can shed the virus for 4-6 months or for a year or more in a continuous or intermittent fashion.Recurrent infections are also common.FECV is readily spread through litter and litter dust, and can be carried from place to place on people's bodies and clothing.Virus contaminated material is easily transferred to the paws and fur of susceptible cats and then ingested during grooming.Kittens are infected by other cats at about 9-10 weeks of age, although one report places it as early as 3 weeks.


FIP is caused by a feline coronavirus. Coronaviruses of various species exist in most types of animals and humans and usually cause acute respiratory or enteric disease. FIP is the cause of death of 1 in 100 to 1 in 300 cats in U.S. The incidence can be 5 or more times greater among young cats coming from catteries and shelters and is the major cause of abdominal fluid (ascites) and intraocular and neurologic inflammatory disease in cats under 3-5 years of age. FIP is virtually 100% fatal and there is no good prevention. The emotional toll of FIP is especially great, because it strikes suddenly weeks, months and even years after initial infection. Therefore, cat lovers usually experience this disease long after they have developed strong emotional bonds with their new pet.

Coronviruses are ubiquitous among all cat populations and the principle one of cats is correctly referred to as feline enteric coronavirus (FECV). FECV is present in virtually all catteries with 6-8 or more cats and up to 40% or so of the kittens relinquished to shelters. The enteric virus in the cat population lives in the digestive tract and is shed in feces. Cats can shed the virus for 4-6 months or for a year or more in a continuous or intermittent fashion. Recurrent infections are also common. FECV is readily spread through litter and litter dust, and can be carried from place to place on people's bodies and clothing. Virus contaminated material is easily transferred to the paws and fur of susceptible cats and then ingested during grooming. Kittens are infected by other cats at about 9-10 weeks of age, although one report places it as early as 3 weeks.

FIP is caused by a mutation of FECV. Although the mutation of FECV to FIPV is common, it is fortunate that only a small percentage of cats exposed to this mutant virus will get FIP.  FECV is undergoing continuous mutation and several genetic forms of the virus may co-exist in the same animal at the same time. Most of these mutations have very little effect on the behavior of the virus and merely serve to genetically reflect the region from which the virus originated. However, certain have a pronounced effect on the biologic behavior of the virus One study indicated that 20% of the kittens infected with FECV will produce an FIP mutant. Of course, only a fraction of the mutants will go on to produce FIP, depending on host resistance factors (genetic or non-genetic).


FIP was first recognized as a specific clinical entity in the late 1950's. This timeline was based on decades of meticulous necropsy records kept by pathologists at the Angell Memorial Animal Hospital. There was a steady increase in the incidence of the disease in the 1960's onward, and it is currently one of the leading infectious causes of death among young cats from shelters and catteries.


FIP affects both pure- and random-bred cats. However, the disease usually starts in young kittens so it is closely linked with cat breeding and sheltering. The disease is also enhanced by improper husbandry, especially resulting from overcrowding (shelters, large multiple cat households). We also know that genetic susceptibility may account for 50% or more of the risk of developing FIP in one pure breed that was studied.


The age of the cat at the time of initial FECV exposure may play an important role in whether a cat dies from FIP. Kittens usually began shedding FECV at around 9-10 weeks of age, which places their actual exposure a few days to a week earlier. The immune system of the kitten is rapidly maturing during the period between 6-16 weeks of age. Therefore, the first exposure of most cats to FIP causing mutants occurs during a time period when their immune systems are still developing. This lack of development enhances the likelihood of a FIPV mutant to gain a strong foothold into the body. Just as there is an age susceptibility, there also appears to be an age resistance. FIP is seldom seen in cats over 3-5 years of age, and most cases occur before 16 months of age.

Anything that stresses cats can depress immunity and also increase the likelihood that FIPV will establish itself in the body. Stress may also allow an FIPV that is being successfully contained to become active. The effect is even more powerful if the stress occurs at or shortly after the time the cat is exposed to the virus. Stressors can include overcrowding, weaning, spaying or neutering, other infections, being placed in a new and strange household, adding new cats to a household, shipping cats to new owners or other catteries, or stresses of pregnancy, parturition and lactation. Disease caused by feline herpes virus and other common upper respiratory pathogens are good indicators of cattery or shelter stresses.


Signs of FIP arise weeks, months, and in rare cases years after initial infection. During this quiescent stage, the cat may be asymptomatic or suffer from vague signs such as stunted growth or increased susceptibility to other common infections. Many believe that FIP can cause upper respiratory disease signs during its early stages; this is not technically correct, because upper respiratory disease is usually caused by herpesvirus, chlamydophilla, mycoplasma, etc., and not directly by FIPV.


Cats with FIP do not appear to be very contagious to cats that they come in contact with. Although this has been based mainly on clinical observations, it has also been confirmed by laboratory studies. Contact transmission has not been observed in experimental settings. Furthermore, cat-to-cat transmission implies that every FIPV isolated from a group outbreak of FIP will be genetically identical. UC Davis researchers have yet to observe this. However, researchers now know that FIPV is present in the feces of some cats with FIP, so horizontal transmission is theoretically possible, and may explain the uncommon epizootics of FIP where a number of cats in the same environment develop FIP within a days or weeks of each other.

There is no single definitive test for FIP at this time, however the diagnosis of FIP should be relatively simple given its affinity for younger cats, its strong tendency to involve catteries and shelters, the typical physical and historical findings, and numerous characteristic laboratory abnormalities. Nonetheless, it remains one of the most difficult of diagnoses for many veterinarians. The truth is that veterinarians have little trouble in placing FIP high, or at the top, of their diagnostic list, but have great difficulty, and even reluctance, in confirming their diagnosis. This is probably because FIP is viewed as a death sentence, and they are reluctant to confer such a sentence without certain proof.


There is currently no cure for FIP; therefore, the primary concern needs to be making the cat comfortable and deciding when to quit. Cortisone can help reduce inflammation and encourage appetite. Good nutrition, hydration and non-stressful environments are also important, but in almost all cases they serve only to prolong the inevitable. Therefore, we will encourage some owners to go with symptomatic treatment, but only if the animals are not suffering. Owners of cats with FIP should be wary of claims for alternative type therapies that are based on anecdotal evidence.


There have been reports that the feline interferon omega is effective in combating FIP. Davis researchers actually tested it against FIP years ago and it did not work. Fortunately, a double blind, placebo controlled study was recently reported from Europe on the use of interferon omega in treating FIP. Cats receiving this very expensive treatment fared no differently than placebo treated cats.



This is a decision only the cat's owner can make, and it is a difficult one. It is not recommended to euthanize a cat, even with FIP, as long as it looks and acts fairly normal. Miracles do happen, but they can't happen unless they are provided time to happen. However, some owners choose to end suffering at an earlier stage, given the grave prognosis. Many owners decide to put an animal down when it no longer takes pleasure in life. But cats can feign health to the last. There is a myth that if a cat is still purring it is still enjoying life. Research has shown, however, that cats purr even when in extreme pain, it is another way that they mask illness.

If you have lost a cat to FIP, remove any cat related items that you cannot wash or disinfect, such as a scratching post or soft toys. Clean and disinfect everything else in the environment that you can. Time will take care of the rest, because viruses of this type are not long-lived in the environment. A couple of months are recommended, which is standard for most infectious diseases.

A vaccine has been developed and is available. However, it has to be used in kittens at least 16 weeks of age (most cats are already exposed to coronavirus at this age), it is not effective in cats already exposed to coronavirus (which is most cats), it is not effective against the common serotype of FIPV, and even when all factors are optimal, it has low efficacy. In short, it does not work in the environments where it is needed most (catteries and shelters) and is not justified in older pet cats where FIP is hardly seen. UC Davis researchers do not recommend its use.

Avoid stress and overcrowding. Keep cats in small, separate groups. Consider isolating kittens from a mother cat at weaning to avoid exposure to the virus. Don't mix very young kittens with older kittens. If you can limit coronavirus exposure until 12-16 weeks of age, when the immune system is better developed, the likelihood of developing FIP may be lessened. Breeders should avoid matings between cats who have had close relatives that have died of FIP or who have produced kittens that developed FIP. Also follow accepted protocols for vaccinations and practice good husbandry to limit other infections. Clean and disinfect cages and litter boxes regularly. The corona virus is easily killed by bleach and other disinfectants.

It is true that there is currently no cure, or totally effective prevention. But researchers understand the virus and the infection much better now. They have new tools that allow them to look at viruses at the molecular level. Any knowledge about the virus and how the host cat responds to it will have influence down the road. The Feline Genome has been sequenced, and with this important new feline DNA roadmap researchers will be able to identify viral genes responsible for causing disease (which will facilitate antiviral drug development) and host genes that confer resistance/susceptibility (which will facilitate genetic control).


All funds given to SOCK FIP for the CCAH will go right into FIP research. Some of this research will be clinical in nature, and some bench top. $50,000 - 75,000 a year supports a single technician or graduate student, and the more such people the CCAH can engage in research the faster we will reach our goals. The genetic testing will be expensive - the DNA chip arrays will cost $400 or more each just to purchase (once they are developed by commercial companies), read, and analyze. As demonstrated by SOCK FIP's predecessor, SOCK it to Leukemia, a great deal of money can be raised by ordinary people), and a lot can be accomplished with that money if it is concentrated in the hands of knowledgeable and capable researchers.

Though SOCK FIP is trying to focus funding on U.C. Davis for greater impact, the scientific community is very collaborative and pedigree/disease information and DNA samples will be useful for meaningful collaborations. UC Davis researchers are also aware that other groups are raising money to study FIP, and this is also respected and accepted. The goal of SOCK FIP and the UC Davis Center for Companion Animal Research is to solve FIP and in the end it really does not matter how it is accomplished or who does it. Scientific competition is always good. A world full of researchers have studied this disease for over 40 years, and although we know a lot more about it, we still do not have effective ways to totally prevent or cure this disease. Hopefully, this worldwide research effort will finally bear the needed fruit. Researchers at UC Davis and the CCAH can only do the best as their part.