In a recent study cats were tested in the same manner as in the vaccine manufacturer’s tests. At the end of an 8-week period, 30% of cats vaccinated, and 60% of the controls demonstrated FIP-positive conditions from tissue examinations. This demonstrates a 50% “preventable percentage.”

Another recent field trial ran for 16 months using 500 cats in a no-kill shelter with endemic FIP. The fact that this is a shelter makes it a different makeup than a cattery (and some multi-cat households) because the average age of a cat was approximately 2 years old, and there were no kittens under 16 weeks old. However ALL cats tested were seronegative prior to exposure in the shelter. During the time of the study, 0.8% of the vaccinated cats died and 3.25% of controls died of FIP. [This is statistically significant at p=.048, which means that there is a 95.2% probability that this result is not random] So, for seronegative cats over the age of 16 weeks, this study shows a 75% efficacy rate. Vaccination after exposure (after a cat is already seropositive) is not helpful in preventing the disease.

Wouldn’t we all like to know! Seriously, there seems to be two schools
of thought. One group (from Cornell-based publications and seminars)
states that the spread is not known with certainty, but is believed to
be by ingestion or inhalation of the virus. The other school of thought
(from Dr. Pedersen and the UC, Davis based publications) believes that
transmission is most prevalent when cats have close contact with other
infected cats or their feces/urine. Both schools seem to feel that feces
may play a large role in the method of transmission.

Some studies suggest that viruses that can cause FIP can survive
on dry surfaces (food/water bowls, litter boxes, human clothing, etc.) and
can survive at room temperature probably up to 2 or 3 weeks. If this is
the case, then the two schools of thought on methods of transmission may
not be so far apart, especially given that litter can contain dust to
which small particles of feces can adhere. Thus the virus can possibly be
spread via litter dust on shoes or clothing or etc. making it behave as if
it were an airborne virus!

Limit the number of new cats and isolate each for at least one month,
preferably two. I know it sounds like a long period of time, but
consider the alternatives! You could lose every cat in your household.
During the one month’s time period, make sure you watch carefully for
signs of illness. You should give the coronavirus titer test at the
beginning and the end of the quarantine period, and the titer should
decrease over that time period.

Scoop the litter box daily, discard the rest of the litter weekly and
disinfect the boxes with a 1:32 solution of bleach. The area around the
boxes should be swept and disinfected, there should be at least one box
for every two cats in the household. Again, weekly discarding of the
scoopable litter may seem like a waste, but so far the ONLY thing the
sources agree upon with regard to transmission is that it is definitely
transmitted through the feces, if nothing else. In the words of one
breeder: “It cost me approximately $3,000 in veterinary and laboratory
services to diagnose the incidence of FIP in my cattery, test and
retest (and retest) all of my cats. Believe me it is FAR less expensive
to discard the litter” (Polli, p. 81). If your cats have long hair and
fecal matter tends to stick to the britches, this hair should be kept
clipped short.

Change food and water daily, disinfect the bowls weekly. Do not mix the
bowls all around the house, keep the same set of bowls with the same
cats, and keep the same set of litter boxes with the same cats.

People often use the “it’s like AIDS” phrase to describe a number of
illnesses in the animal (and human) community with the idea that most
people know so much about AIDS that this analogy is useful.
Unfortunately most people don’t know much about AIDS and the resulting
effect is to scare people out of their wits and have them dump their
cats or dogs at the nearest pound because they are so deathly afraid of
catching AIDS from them. The ONLY similarity between FIP, FIV (Feline
Immunodeficiency Virus) and FeLV (Feline Leukemia Virus) to HIV (which is
believed to cause AIDS) is in their genetic makeup. All are RNA (as
opposed to DNA) viruses, and FeLV and FIV (and HIV) are what are known as
“retroviruses.” FIP is a type of “coronavirus” which makes it even less
similar to HIV. To make it clear: THERE IS
ABSOLUTELY NO WAY TO CATCH AIDS FROM A CAT, NO MATTER WHAT FELINE
DISEASE THAT ANIMAL MAY HAVE. See the FeLV FAQ for more
information on retroviruses.

Most household soaps, detergents and disinfecting agents will
kill the virus. Make sure you wash any part thoroughly that has come in
contact with the cat (don’t forget your pants if the cat rubbed up against
you). Bleach in a 1:32 solution is suggested for decontamination
purposes.

Understanding Feline Infectious Peritonitis
Niels C. Pedersen, DVM, PhD

Dr. Niels C. Pedersen is Director of the Veterinary Genetics Laboratory and Director of the Center for Companion Animal Health at the University of California at Davis. Dr. Pedersen is an international authority on infectious diseases and immunological disorders in small animals and in comparative genetics. His current areas of research focus on infectious diseases of cats and dogs in shelter and multi-animal environments, and on applied feline and canine genetics.

What is Feline Infectious Peritonitis – FIP?
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 cats seen at veterinary teaching hospitals throughout the U.S. The incidence can be 5 to 10 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.

Does FIP only affect pedigreed cats?
FIP affects both pure- and random-bred cats. However, the disease usually starts in young kittens, so it is closely linked with cat breeding. 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. Although FIP occurs in all breeds, there is no doubt that certain bloodlines, and therefore certain matings, are more apt to produce kittens that eventually die from FIP. These genetic factors are most likely a result of the inbreeding that goes into breed development. Therefore, catteries are at the highest risk because they are subject to all three risk factors (kitten production, dense housing, genetic susceptibility). The likelihood that any given cattery will suffer at least one outbreak of FIP over a five year period is very high, and mortality in catteries can be 5-10 times higher than it is in the general population. Shelters have the second highest risk, and the greatest incidence is among kittens adopted during periods of overcrowding and prolonged stays. Most shelter kittens are random bred, with many coming from the feral cat pool. Random bred kittens are more genetically diverse in general, so husbandry factors are more important in causing FIP in this population than genetic factors. Husbandry factors are greatly influenced by the seasonal influx of kittens.

Why are you particularly interested in cats and FIP?
I was raised on a poultry farm in southern California. My dad fed many feral cats so they would stay around and keep the rodents down. As a result, I experienced and loved cats for as long as I can remember. When people came to the farm to buy eggs, I would sit with a box of kittens to give away, and sometimes I would get 25 cents for a kitten, which at the time I thought was a fortune. At first I wanted to be a cattle doctor, because I also grew up around beef and dairy cows and had show steers in high school. But when I went to veterinary school, I discovered that nobody knew much about cats and cat diseases. In those days there were lots of deaths associated with feline leukemia virus, but of course we did not know this virus existed until several years later. But from the beginning I had the most fascination for FIP. The first reported clinical cases of FIP were in 1963. My first publication on FIP was in 1965. I’ve been a member of the faculty at Davis since 1972.

What is the History of FIP?
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. The reason for the sudden emergence of FIP is not known, but there are at least two possible explanations. First, it is noteworthy that FIP appeared within a decade
of the initial descriptions of transmissible gastroenteritis (TGE) of pigs in North America. The causative virus of FIP is closely related to TGEV of pigs and canine coronavirus (CCV), although they are still genetically distinguishable. However, mixtures between these three viruses are known to occur. At least one strain of canine coronavirus can induce mild enteritis in cats and enhance a subsequent infection with FIPV, indicating a special closeness to feline coronaviruses. Therefore, CCV may be a more likely parent of FECV in this scenario. Another related possibility is that the FIP mutation occurs only in a relatively new strain of FECV, and that this new strain only evolved in the 1950’s. Coronaviruses such as FECV are continuously mutating as a result of the manner in which their genetic material (RNA) is replicated. Therefore, genetic change, either among themselves or through genetic mixing with closely related coronaviruses from other species, could have either allowed a coronavirus of another species to take up host in cats or to alter a strain that existed prior to the 1950s.
An alternative non-genetic explanation may involve changes in how cats were viewed as pets and their husbandry. There was a dramatic shift in the status, keeping, and breeding of cats as pets after WWII. The numbers of pet cats greatly increased, purebreeding and cattery rearing became increasingly popular, and more cats, and in particular kittens, found themselves in shelters. These large multiple cat indoor environments are known to favor feline enteric coronavirus (FECV) infection and FIP. Interestingly, feline leukemia virus (FeLV) infection also became rampant among indoor multiple cat households during this period, and FeLV infection was a significant enhancing factor for FIP until it was pushed back into nature as a result of testing, elimination/isolation, and eventual vaccination in the 1970s and 1980s.

How is the coronavirus spread between cats?
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 in 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 easily 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.

How does the coronavirus turn into FIP?
FIP is caused by a mutation of FECV, which is ubiquitous among cats. 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, mutations that inhibit or knock out the function of a certain small gene (called 3c) have a pronounced effect on the biologic behavior of the virus. All known isolates of FIP virus that we have studied, and that have been reported by others, have various types of mutations in the 3c gene. Mutations within the 3c gene with the potential of causing FIP are common. 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). This FECV to FIPV genetic change is referred to as the internal mutation theory. The internal mutation theory has two corollaries: 1) that each cat that develops FIP, even if it is a littermate, closely related or commonly housed, has a different mutation in the 3c gene, and 2) that horizontal (cat-to-cat) transmission of the FIPV mutant is uncommon. We have reconfirmed corollary 1, and have confirmed corollary 2 in concept but not in fact. Reconfirmation for the internal mutation theory came from a recent outbreak in three kittens in a litter of Scottish Folds and in a half-sibling from a second litter. All four FIPVs had significant, but different, mutations in their 3c genes, but were closely related in all of their other genes to one of two different FECVs detected in the feces of one of the kittens. We have found that many cats with FIP are in fact shedding the same FIPV in their feces that is in their diseased tissues. However, for some reason, it does not appear to be highly contagious.

What are the signs of FIP?
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 breeders and even clinicians 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. With time, many cats win their battle with this infection, while others lose. However, “losing the battle” may occur over a very long period of time; only terminally, when the cat’s defenses collapse, do the more characteristic signs of FIP develop. This capitulation to the virus explains why cats with FIP seldom recover, because a loss of immunity is extremely difficult to reverse. Cats who develop clinical cases of FIP may initially show nonspecific symptoms such as loss of appetite, depression, rough coat, weight loss, a fluctuating antibiotic resistant fever, and increased susceptibility to secondary infections (such as respiratory disease). More specific signs of FIP vary depending on the form of the disease (wet vs. dry) and the organs that are involved.
The most common form of the disease is referred to as “wet FIP.” Wet FIP is caused by inflammation of the linings of the abdominal viscera, and less commonly of the thoracic organs. This inflammation exudes large volumes of a characteristic mucinous, yellow-tinged fluid (exudate). Therefore, the major clinical sign in the wet form of FIP is ascites and abdominal distension (abdominal involvement) or dypnea (thoracic involvement).
FIP can also take a more chronic form referred to as “dry FIP.” Dry FIP, as the name implies, is not associated with fluid accumulations in the abdomen or chest, but rather with more localized masses in the kidneys, spleen, liver and terminal bowel, eyes, and the linings of the lungs and heart, and central nervous system. Uveitis (intraocular inflammation) can affect the eyes, making them look cloudy and changing the color of the iris. Inflammation can enter the brain and spinal chord and cause a spectrum of progressive neurologic abnormalities. FIP accounts for over one-half the cases of inflammatory intraocular and nervous system disease in cats under 3-5 years of age. Although unappreciated in the past, we now know that cats in the terminal stages of FIP are often severely immunocompromised. This explains why common bacterial infections may complicate the disease picture in cats with FIP.

Is FIP contagious?
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. We have not observed contact transmission in experimental settings. Furthermore, cat-to-cat transmission implies that every FIPV isolated from a group outbreak of FIP will be genetically identical in its 3c gene mutation. As I mentioned earlier, we have yet to observe this. However, we now know that FIPV is present in the feces of most cats with FIP, so horizontal transmission is theoretically possible, although very uncommon.

How do genetics, stress, and other infections play a role in FIP?
FIP is not a breed specific disease, but does follow certain bloodlines within breeds. Heritability accounts for about 50% of the incidence. Environmental factors influence the other half.
The age of the cat at the time of initial FECV exposure plays an extremely 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.
In the 1970s, when tests for FeLV became available, we discovered that one third to one half of all cats with FIP were also FeLV positive. In later experiments, we showed that cats that had resisted infection with FIP virus would develop FIP shortly after being infected with FeLV. This meant that FeLV infection somehow interfered with the ongoing immunity to FIPV. With the elimination of FeLV as a major infection of cats, we no longer see such a strong relationship, especially among catteries and shelters where FeLV control programs are in effect. Most cats with FIP in the present age, with the exception of a few household pet cats, are not FeLV infected.
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. If a cattery or shelter is having a lot of problems with these upper respiratory infections, it is likely that they will also have problems with FIP (especially if the genetics are unfavorable as well). For instance, an area SPCA had a huge FIP problem in the kittens they were adopting out. It was kitten season and the facility was overcrowded with cats and they had to stay for longer periods awaiting adoption. There was also a lot of upper respiratory disease. After limiting their intake of cats, overcrowding was eliminated and cats were adopted after shorter stays. The FIP problem decreased to negligible levels, as did the respiratory infections.

Is there a definitive test for diagnosing FIP?
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 somehow 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 we are reluctant to confer such a sentence without certain proof.
Although a definitive test result would assist decision making, a certain diagnosis can be based on cumulative odds rather than a single, simple, definitive test result. A young cat from a cattery or shelter with chronic uveitis and/or neurologic signs, high serum proteins, hyperglobulinemia and hypoalbuminemia, fluctuating antibiotic unresponsive fever, leukocytosis with a lymphopenia, and an anemia of chronic disease can have no other disease than dry FIP based on odds alone. Likewise, the same cat with similar history and laboratory findings, but with yellow-tinged, mucinous, inflammatory ascites is highly unlikely to have any other disease than wet FIP. It is interesting that a cattery owner or cattery worker is often the one to cue in on the correct diagnosis based on the simplest of observations and intuition.
In an attempt to reach the elusive definitive diagnosis, veterinarians rely on dozens of tests that claim to highly correlate with the disease or to be diagnostic. I do not have time to go into the dozens of tests that fall into this category, or the good tests that are improperly done, or improperly interpreted, that lead to misleading positive or negative results. In truth, the only good definitive way to diagnose FIP is to identify the virus in macrophages within lesions or ascetic/pleural fluid by a procedure called immunohistochemistry. PCR would work equally well on diseased tissues or fluids, but many of the current tests are improperly designed and conducted and frequently yield misleading results. In some cases, the proper fluid or tissues cannot be obtained pre-mortem. However, there is no excuse for not doing such definitive tests post-mortem.
This brings me to a final point, a necropsy should be done by a qualified veterinary pathologist on any cat that requires a proper diagnosis. However, even veterinary pathologists will hem and haw about a definitive diagnosis, even when faced with incontrovertible historical, clinical and histological evidence. Make them make a definitive diagnosis, either based on proper reading of the odds or by doing immunohistochemistry on lesions.

What is the best way to care for a cat that has FIP?
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. There have been reports that the feline interferon omega is effective in combating FIP. We 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 will hopefully stop the use of this treatment in the US and other countries, although some people still believe more in anecdotes than scientific trials. Unfortunately, veterinary medicine is filled with anecdotal treatments.

How do you know when to euthanize a cat that has FIP?
This is a decision only you can make, and it is a difficult one. I would never suggest euthanizing 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, I also cannot argue with those owners that decide to end suffering at an earlier stage, given the grave prognosis.
I always tell owners to decide to put an animal down when it no longer takes pleasure in life. But cats can feign health to the last moment and you often regret in retrospect not making the decision earlier. I did the same thing with one of my cats that was dying of cancer. He actually was dead one morning, even though I still thought he had time to live and seemed reasonably content. There is also a myth that if a cat is still purring that it is still enjoying life. But research has shown that cats purr even when in extreme pain, it is another way that they mask illness.

After you have had FIP in an environment, how long should you wait before a new cat or kitten is brought in, and what other steps should you take?
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. We generally recommend a couple of months. These steps are undoubtedly an overkill when it comes to FIP, but these recommendations are standard for most infectious diseases and we try to keep everything simple and consistent.

If FIP occurs in a cattery, how do you decide whether and which cat to spay/neuter?
We know that genetics play a strong part in FIP – at least 50% of the incidence or more has a heritable component. We know that susceptibility is carried both in paternal and maternal lines, but we have suggested, at a minimum, that paternal lines that throw kittens that die from FIP not be used for breeding. This is because toms breed multiple queens and sire dozens or hundreds of kittens, and have the greatest influence on how bloodlines are developed. This is true of a lot of diseases – the “Founder effect.” If females are genetically weak, and bred to weak toms, that is when you get into problems. If toms are genetically strong, and queens are genetically weak, the male’s resistance genes seem to mask this weakness. The best scenario is to not breed either susceptible toms or queens, but not using problem toms is the best possible alternative in the interest of doing the most with the least disruption of breeding practices and bloodlines. However, if there are multiple losses from FIP in a litter, remember that susceptibility comes both from the paternal and maternal lines. It’s also important to consider the cat – if you believe the cat may be at risk for FIP, avoiding the stress of being a breeding cat may help prevent the disease for that individual.

If one kitten in a litter has FIP, how likely is it that other littermates will be affected as well?
We know that if one kitten in a litter gets it, that the others are several times more likely, but this is not absolute. If the overall incidence is 5% across the spectrum of young cats produced in a cattery, it could be 10-50% or higher among the remaining littermates. I have seen one kitten in a litter of 6 killed by FIP and I have also seen 5 out of 6 develop the disease. Time is the only thing that will determine the fate of healthy siblings.

Sometimes both bacterial and viral infections exist in a cat with FIP – which came first?
It is really impossible to say which came first, because it is like chickens and eggs. A given cat could have had some underlying immunosuppression that made it susceptible to a number of common feline pathogens as well as FIP. It is also possible that the cat suffered from FIP for a long time and that this was the cause of immunosuppression and the other infections were secondary.

What is the best way for breeders to prevent FIP?
Resistance is the ability of the immune system to cope with a disease. We know that 50% of the incidence is heritable, and we know that resistance (or susceptibility) factors exist in both toms and queens. However, culling problem toms is the simplest genetic procedure to reduce incidence. Toms produce far more litters and kittens than queens, and therefore have a much bigger effect on the disease. Good judgment and husbandry will influence the other 50% of the equation. Pick the largest and strongest in a litter to keep for breeding and avoid kittens that are slow growing and prone to other infections. Spay and neuter cats that throw FIP and adopt them into good homes. Avoid stress and overcrowding; maintain only those cats deemed necessary for your breeding program and chose mating wisely to limit kitten numbers. Keep cats in small, separate groups. Consider isolating the kittens from the mother 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 will be less. 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.

Is it possible to have a corona virus free cattery?
This is extremely difficult, because the virus is ubiquitous in the environment and easily spread by cats and on people. Isolation of queens and early weaning has been touted in the UK and is used in the US. However, UK catteries are small and such a program can only succeed in smaller catteries and with exceptional isolation facilities and quarantine procedures. Moreover, even if you could produce a virus free cattery environment, the moment a kitten or cat goes to new environments such as a pet home it will most likely be exposed to FECVs. Therefore, we do not recommend this procedure unless simpler husbandry practices totally fail to reduce the problem.

Isn’t there an FIP Vaccine?
A vaccine was 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. We do not recommend its use.

Why is there hope now for progress on finding ways to prevent and treat FIP?
It is true that there is still no cure, or totally effective prevention. But we understand the virus and the infection much better now. We have new tools that allow us 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 in 2 years it will be complete. We 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).
There are only two ways to affect the corona virus at the current time – through husbandry and careful matings. Husbandry techniques can help prevent the spread of the virus – a great deal of research has been done and continues in this area at the Shelter Medicine program at Davis.
Understanding how the immune system affects both resistance and the form of the disease (wet vs. dry) will be important. Immunity studies focus on how to modify the immune system’s reaction to the virus. Understanding how to block inflammation and the development of anti-viral drugs would be ways we could fight it. There is no reason why these can’t be developed. In fact this was happening following the appearance of the severe acute respiratory syndrome (SARS) – another coronavirus disease, but of humans. However, this research was curtailed when SARS failed to spread to the general population and was easily contained. But it made human researchers interested in the corona virus. Drugs could be developed and used in FIP with some effect – like HIV/AIDS it could become a manageable disease
If we can discover the genetic basis for susceptibility, we will be able to offer genetic testing and breeders can breed out the trait over several generations, while preserving valuable bloodlines. This is exactly what breeders are doing with many other genetic diseases, such as polycystic kidney disease in Persians and breeds with Persian blood.

How can Burmese and Birman breeders help with FIP research?
Genetic research has great potential, but it takes time and money. Because FIP is a purely animal disease, there will be limited funding from sources such as the NIH. It’s important to start banking DNA and assembling pedigrees showing relationships between affected and healthy cats. Breeders should not be ashamed of FIP. If you breed enough cats, long enough, you will experience FIP. The reluctance of breeders to talk about it has been a huge detriment to FIP research. For instance, if every one would cooperate, we could determine whether or not there is a genetic basis for FIP resistance or susceptibility in rapid time. If there is a genetic basis, we could then determine the gene or genes involved and develop tests to predict which cats to breed or not to breed. Fortunately, some breeders are now coming forward and cooperating in raising funds for FIP research and providing information and materials (such as DNA and FIP virus isolates) from the field. Such people have come out in the past, but they usually get frustrated and give up after a while. So if we want to succeed in understanding this disease we must all work on together to collect the DNA, case and pedigree information that will help us advance our research.
FIP affects all breeds, but we cannot spread our genetic studies across all breeds. We only need two breeds, which are inbred to a degree and have relatively small to moderate numbers in their registries. We have seen a number of FIP cases in Burmese and Birmans this year, especially in certain bloodlines. Burmese and Birman breeders seem to know a great deal about bloodlines and certain matings that result in FIP. Because Burmese breeders have cooperated so well on the head defect project, they know what is needed for another genetic study. Birmans do not have head defects, but Birman breeders appear equally involved and knowledgeable about the genetics of their breed. We are trying to get as many breeders of these cats as possible to come together and provide at least three generational pedigrees, with DNA samples (cheek swabs with Q-tips), of families known to produce affected kittens. These families are essential for determining the genetic basis for FIP susceptibility
We need FULL cooperation from breeders of these two breeds. We can code the information we receive – so confidentiality will be maintained. It’s my hope this will reassure breeders to provide us with full data and pedigrees on FIP cases and related cats they have experienced in their catteries.
There are two types of studies we want to do. Whole genome linkage mapping requires at least three generations of cats with 30 or more members and with accurate identification of FIP affected and non-affected individuals. Similar information can be obtained by combining information from a number of smaller families, providing breed pedigrees are made available to determine degrees of relatedness among these families.
Whole genome association mapping involves two large groups of cats of the same breed – one group of cats that have had FIP, the second that have not had the disease. This can be two different catteries, one with problems and one without (but please be honest about your status, as false classification will doom this type of study). These two groups can also come from different bloodlines in the same cattery – breeders have strong intuition on which cats are problems and which are not. We need a total of 100 or more cats in each group (affected and non-affected) for association mapping.
Breeders, besides information from your cattery, talk to clients. We want information on siblings and parents and grandparents of FIP cats. Get DNA on everybody in your cattery and from relatives whenever possible. Now is the time to start to collect and bank DNA for when the feline genome is complete. It is also important for future research on other feline diseases.
We will also need fecal samples to collect viral RNA for studies on the origins of FECVs and FIPVs. We need to know if certain strains of FECV are more apt to mutate to FIPV, and if catteries having these strains are therefore more likely to suffer high FIP loses. It is extremely important that FIP is accurately diagnosed. We can help to review veterinary records to see if there is enough evidence to confirm the diagnosis. We can accept proper tissue samples taken at necropsy or biopsy from your veterinarians and test them for FIP. We can also do necropsies at Davis when possible and necessary.

How much money is needed for this research at Davis?
All money given to Davis will go right into FIP research. Some of this research will be clinical in nature, and some bench top. We need $50,000 – 75,000 a year just for a single technician or graduate student, and the more such people we 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. These are certainly daunting figures, but doable if everyone admits to their problems and work together. As demonstrated by our predecessor, SOCK it to leukemia, a lot of money can be raised by ordinary people (cat breeders, cat owners, cat lovers), and a lot can be accomplished with that money if it is concentrated in the hands of knowledgeable and capable researchers.

What about other universities and institutes that are studying FIP?
Though we are trying to focus 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. We are aware that others are interested in this same approach. Our goal 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. We are also aware that other groups may be raising money to study FIP, and this is also respected and accepted. 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. We can only do the best as our part.

My heartfelt gratitude to Dr. Pedersen for answering my many questions about the disease – questions I know are shared by others. I believe the comprehensive information he has provided will help breeders, rescue and shelter workers, veterinarians, and cat lovers in general to gain a better understanding of FIP and ways to prevent it in our cats. I also hope it will encourage Burmese and Birman breeders and fanciers to participate in this important research.
Nancy L. Reeves, United Burmese Cat Fanciers

If your cat comes in regular contact with other cats (i.e.: a multi-cat household), the answer is YES! The lowest risk groups are indoor only, single-cat households. The higher the number of cats, the more risk of FIP. The higher the number of cats, the higher the titer test results (more on titers below). Single-cat households are generally free of all coronaviruses. FIP occurs in greatest incidence in cats between six months and two years old, although infections are high up to five years old. Of course the most susceptible group to catching FIPV are kittens because under the age of 16 weeks their immune system is very bad in general. Studies also show that poor nutrition, high stress levels or poor husbandry increase the likelihood of getting FIP. Outside exposure, exchanging of animals, especially kittens and young cats, highly inbred cats, and cats in actively breeding households increase the risk. Males and females are equally affected. There also appears to be a genetic component to FIP that may put some family groups at a particularly high risk.

There is a test which will look for the presence of coronavirus
antibodies in your cat’s blood. If your cat has been exposed to a
coronavirus, ANY coronavirus, its immune system will build up
antibodies to it, and the titer tests for the level of those antibodies
in the blood. But it does not distinguish between antibodies made
specifically against FIP, or FECV, or any other coronavirus. A
positive titer means only that your cat has created antibodies
(therefore been exposed to) SOME form of coronavirus. The higher the
titer, the more antibodies the cat has created.

As if there were not enough problems with the
coronavirus test, there
is no uniformity between different labs. One cannot compare results
from one lab to another. Some labs just specify positive or negative if
the results are above or below a given titer (often these labs do not
even specify the titer). There are no standards for setting up a lab,
there is no regulatory body that oversees them, and no requirement for
validation of test results. It is also possible for a cat which has
received the vaccine (more below) to have enough antibodies to appear
on the titer test. To top it all off, false positives occur in up to
30% of the tests. In sum: DO NOT PLACE MUCH CREDENCE IN THE TITER TEST,
AND UNDER NO CIRCUMSTANCES SHOULD A CAT BE EUTHANIZED BASED SOLELY ON
THE RESULTS OF THE TITER TEST.

There are some clinical indicators which your vet may discuss with you
if s/he suspects that a cat has FIP, particularly if it is showing
likely symptoms. Some blood tests can help your vet pinpoint FIP as a
cause for your cat’s condition, this includes looking for a high amount
of gamma globulin proteins and a low amount of albumin proteins in the
blood.

There has also been talk of a polymerase chain reaction (PCR) test, in
the hopes that it can tell the difference between FIP and other
coronaviruses. Significant scientific studies have yet to be concluded
on this method. However, given that the most common way of a cat
coming down with FIP is via the mutation of FECV, this test may have
little or no value in the great majority of cases.

A 1992 study found the following: 400 kittens were divided into 41
household with various FIP histories. In one group the kittens were
allowed to freely associate with all the cats. In a second group the
kittens were isolated only with their mother. In the third group, the
kittens were isolated by themselves starting at age 2-6 weeks. Only in
this last group did all of the kittens remain seronegative for any/all
coronaviruses.

Usually by the time the vet is able to pinpoint FIP as the cause of
your cat’s condition, the cat is pretty far along. So long as your cat
is in pretty good shape, not in any pain or discomfort, there is no
reason to euthanize it. Even if your cat is happy and healthy, however,
you MUST make sure you keep it indoors and away from other cats. If you
feel that this will be too great a compromise on its quality of life, it
is better to euthanize it. Since the cause of transmission
is not known, by allowing your FIP+ cat outside, you could cause
numerous other cats to become ill, and even further spread the disease.
But please keep your cat’s welfare foremost in your mind. When its
systems begin to fail, when it is in obvious discomfort, you are only
making things worse by delaying the inevitable. Keep him or her as
happy and as comfortable for as long as possible, that is unfortunately
the only solution at this point.

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

Intro
-----
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%).

Diagnostics
-----------
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
there.

Epidemiology
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.

Prevention
----------
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

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

Intro
-----
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%).

Diagnostics
-----------
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
there.

Epidemiology
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.

Prevention
----------
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

Well, Cornell concluded from the above that vaccine efficacy in a
laboratory setting is highly dependent on the challenge. It offers
protection at low challenge doses, none at higher doses. The problem is,
no one
knows what the “real world” dose level is.

Another problem is that there are actually two strains of FIPV. Just as
there are many different flu strains or cold strains which cause you to
get sick several different times with the flu or a cold, because each
time you catch a different strain for which you aren’t already immune.
Type I strain of FIP is believed to be the most prevalent in the “real
world” but it is the most difficult to reproduce in a laboratory. Type
II is easier to reproduce, but not as prevalent outside. It is not
known how effective a vaccine against one type will be against the
other type.

So, while some of the studies have found the current vaccine effective
against the Type II strain of FIP, there is no evidence either way as
to if it will work against the Type I strain.

The consensus arrived at the seminar sponsored by the Winn
Foundation on FIP/FECV is that the enhanced disease effect is a laboratory
phenomenon, especially since that study by Cornell only used seropositive
cats in the first place.

FIP is not caused by a retrovirus but by a type of coronavirus.
One of the reasons FIP is such a problem for vets is because there may be
no way to differentiate an FIP virus from certain other viruses. Current
thinking is that FIP is caused by a mutation of the Feline Enteric
Coronavirus (FECV). FECV is very common, and an FECV infection can have
symptoms ranging from none, to flu-like with or without diarrhea. These
are most common in kittens, but can occur in cats of any age. If the
immune system is not functioning properly, a mutant FECV can become a more
systemic infection that we call FIP. All FIP tests appear to react the
same way to every type of coronavirus. So, if your cat had FECV as a
kitten, it may cause the same reaction in the current test as true FIP
(more on the tests below).

For the purpose of this FAQ, however, I am going to continue referring
to an “FIP Virus” or “FIPV.” Just keep in mind that in fact, there may
not be a difference between FIPV and FECV per se, just a difference in
the way a cat’s immune system responds.

In sum, if you know your cats are seronegative, and they are
older than 16
weeks, the vaccine is recommended by both the Cornell Feline Health
Center and the consensus reached at the Winn Foundation sponsored
FIP/FECV seminar. If your cat is already seropositive, there is not
much evidence that the vaccine will help.

The vaccine will be more of
a help when

• the manufacturers demonstrate its effectiveness
  against the Type I strain of FIP
• it is shown to be effective in
  seropositive cats, and
• it could be shown to be safe and effective for
  kittens under the age of 16 weeks.

However, it appears that there is work being done to develop a
FECV vaccine. Preventing FECV infections in the first place, and
thus preventing FECV from mutating into FIP, might turn out to be
another technique in trying to protect against FIP.

Nobody says a breeder HAS to do any of this. These are merely the
precautions currently recommended by the Cornell Feline Health
Center and the recommendations which came out of the Winn
Foundation sponsored Seminar on FIP/FECV. It is an option kitten
buyers can use in determining which breeder to select if they so
choose, but it is by no mean mandatory.

There is a vaccine available, but it is controversial and some vets
do not recommend it, although others highly encourage it. The
manufacturer’s tests state that it has an efficacy rate (protection
rate in this case) of 69%. Cornell Feline Health Center then did a
study which said the vaccine failed to show any protection, and that it
accelerated the disease in 52.5% of exposed cats. However, this study
used a different challenge virus strain and the route of administration
was different than the manufacturer’s tests. The ‘real-life’
significance of this has not yet been determined, neither Cornell nor
the manufacture has received reports from the field of abnormally high
numbers of cats which get the disease as a result of the vaccine.
However, this study has caused a lot of people to swear-off the
vaccine.

It really is between an individual cat owner and their vet to determine
the whether or not to vaccinate based on the best information available
at the time.

FIP is a disease. Normally the disease/virus relationship is
simple, but this is not the case with FIP. FIP may be caused by many
things, perhaps an isolated FIP virus (FIPV), perhaps a mutation of FECV,
or perhaps there are multiples viruses which can all lead the the same
disease complex known as FIP. There is little question, however, that the
most common cause of FIP is via FECV.

For the most part, FECV is limited largely to the intestines and is
dealt with quite well by the
cat’s immune system. However, as recent studies seem to indicate, FECV
can mutate into FIP and, if the cat’s immune system is not operating
properly, this mutant FECV stops being just an infection of the
intestine and becomes the more systemic infection we call FIP.

Thus, wherever you have FECV you could have FIP! Some cats never
get FIP, but can continue to shed the FECV virus (now thought to be
spread via the feces). The good news, however, is that since it
seems that the dry form is becoming more prevalent, that cats are
gradually becoming more able to resist FIP infection in general.

FIP usually appears in one of two forms: Effusive (wet) and
Non-Effusive (dry). It should not be thought, however, that there are
two different FIP diseases. The results of the infection are a
continuum on a scale, with the ‘wet version’ being one end, the ‘dry
version’ being in the middle, and a ‘carrier’ being the other end (a
carrier is where the cat has successfully fought off the disease but
may still be able to expose other cats to the virus). The way this
happens is when a cat is exposed to FIPV, if its immune system gives a
poor response, the wet form will develop. If it gives a better
response, the dry form will develop. In the best responses, the cat
will not develop either form of FIP, although it may be a carrier of
the FIP virus.

Wet

The wet form is more common, and more rapid in progression than the dry
form. It is characterized by the abdomen and/or chest progressively but
painlessly distending with fluid. If this occurs in the chest,
respiratory distress can occur due to compression of the lungs and
release of fluid into the airways. The lining of the affected cavity
will be covered with white, fibrin-containing areas (fibrin is a
protein that is the center of a blood clot), often on the liver and
spleen. Certain types of lymph nodes may be enlarged. Other signs
include jaundice; mild anemia; and gastrointestinal, ocular (e.g. eye
ulcers or severe conjunctivitis), and neurological signs may also occur.

Dry

The dry form is more rare (but appears to be becoming more common), and
more slow in progression, often making diagnosis difficult. There is
minimal fluid build-up, although weight loss, depression, anemia, and
fever are almost always present. Signs of kidney failure, liver
failure, pancreatic disease, neurologic disease or ocular disease may
be seen in various combinations. Often the organs in question
develop a characteristic pyogranulomatous inflammation (this is a chronic
inflammation resulting in a thickening of the tissue and local
accumulation of white blood cells). Unfortunately biopsy of these lesions
is the only definitive way to diagnose this form of FIP and is usually
done in the form of a post-mortem diagnosis.

It is suggested that queens be completely isolated from other cats
(isolated in its own room, not its own cage within a room). This room
should be empty for one week prior to placing the queen there, and
should be disinfected with a 1:32 solution of bleach. The queen should
be placed in the isolation room 10-14 days prior to delivery. All bowls
and litter boxes should be used exclusively for that room, and not
interchanged with any others. You should disinfect your hands when
entering and leaving the isolation room. If possible, you should even
try to have separate clothing, such as a smock and slippers which are
restricted to the isolation room to decrease risk.

If the queen is not seronegative, you may want to consider an early
weaning program. The queen should be removed from the kittens at age
4-6 weeks and never returned. During the first 4-6 weeks of a kitten’s
life, it gets its antibodies from their mother, therefore they are
immune to anything she may be shedding. After that time period, they
start making their own antibodies. If the queen is a carrier of
coronaviruses, she can shed FECV to the kittens, and they are most
likely to become infected during that time period. Regardless of
whether the kittens are weaned early and isolated from the mother, they
should be kept isolated from all other cats in the household. In
addition to minimizing the risk of the kittens developing FIP, the risk
of exposure to other viruses and diseases will be reduced.

Kittens should be raised in complete isolation from the queen and all
other cats/kittens in the household until they leave the cattery. If
the kitten is to be kept in the cattery, it should be isolated for 16
weeks, and then the FIP vaccination series should be completed before
allowing the kittens to interact with the other cats.

Some cats test positive on the coronavirus titer test, some do not.
Those which have never been exposed to ANY form of coronavirus are
called “seronegative.” Those which have been exposed to some form of
coronavirus are called “seropositive.” The Winn Foundation-sponsored
research felt the
Cornell study was flawed because it used cats which had already been
exposed to some form of coronavirus (were “seropositive”) and then
attempted to test the vaccine.

This is not to be confused with the terms “FIP negative” and “FIP
positive” which are used by many labs to indicate that the
coronavirus titer is less than (negative) or more than (positive)
some predefined threshold level.

The purpose of this FAQ is to answer frequently asked questions about Feline
Infectious Peritonitis (FIP), which is one of the most difficult diseases in
the feline community today. This FAQ is divided into two parts, the first is
general information about the disease, and the second is about management of
FIP in a multi-cat and cattery environment. The sources for this FAQ are
listed at the end, as well as some additional recommended readings.
Recently an excellent source of information on FIP has become available on
the WWW as well. This article is much more technical and many cat owners
may find it much more dense than this FAQ.

I want to point out first and foremost that I am not a veterinarian,
nor even a person who has training in animal science such as a veterinary
technician. I am a graduate student of physical anthropology, and an
ailurophile. My goal with these FAQs is to take information from the
medical literature and convey the parts that are most useful to the
average cat owner and translate them into general terms that are easy to
understand. I attempted to keep the FAQ as untechnical as possible, but
unfortunately with such a complex disease that becomes very difficult. I
hope this prooves to be of some usefulness. Also keep in mind that this
disease is one of the most controversial subjects in feline health care.
This is not a definitive guide to FIP, but only an attempt to compile
the most current information. Ideally the reader of this FAQ should
use this as a starting point when discussing FIP with their veterinarian.
Vets and breeders will hold a wide variety of opinions on this disease,
some of which may be based on current information, some of which may be
based on hearsay and anecdotal evidence. You can only do your best to
become as educated as possible and make your decisions on the course of
treatment or preventive care. Always remember, your cats is YOUR
responsibility, and no one, not your vet, not a breeder, not a
friend-who-knows-everything-there-is-to-know-about-cats, nor the writer of
an internet FAQ can force you do take an action that you don’t feel
comfortable with. Do what you think is best for your cat. Period.

Summary

To begin and unfortunately in sum: There is NO effective treatment, there is
NO diagnostic test, there is NO way to positively identify asymptomatic
carriers (cats which shed the virus, but do not themselves show outward
signs of illness), the incubation time is UNKNOWN, NO one is 100% sure of
how it is spread between cats, and there is NO proven effective way to
control its spread in a multi-cat household or cattery. So what is known?
Read on.