Lorraine Sheltons notes on FIP (year 2004) Feline Extravaganza at UC Davis:

Dr. Niels Pedersen DVM Ph.D.

FIP is a complicated disease. He started studying it in 1964. Causative agent of SARS is a coronavirus, renewing interest in FeCoV. Serotypes: Type I FeCoV (cat-like) 80-90%, Type II (dog-like) 5-20%, Type III? (Pig-like) rare. Swap genes with each other during cross-infections. Biotypes: enteric coronavirus (99%+) and FIP (<1%) can be seen in all three.

FIP a mutation of enteric coronavirus. 5-10% likelihood of mutation occurs mainly during primary FeCV infection (when kittens not fully immunocompetent). Only half or less of kittens with mutation get FIP. Mutation is simple deletion of insertion in 3c gene. It allows virus to infect macrophages, spreading the virus everywhere in the body. The disease symptoms of FIP are caused by the cat's immune attack of these macrophages.

Cats with FIP do not spread the mutated virus, but rather secrete the parent coronavirus. Immunocompromise a cat, expose to coronavirus, develop FIP mutations and FIP. Coronavirus strains from each cattery are identical, but distinguishable from strains in other catteries. FIPV strains are always identical to FeCV strains in the same environment.

Are some strains more apt to mutate and cause FIP than others? Don't know yet. All catteries with more than six or so cats have FECV. Number of cats over 8 do not change incidence of FIP.

FECV has strict tropism: only grows in tips of epithelium of intestinal villi. FIPV has strict tropism to macrophages and is highly pathogenic. Antibody mediated immunity helps to clear FECV from intestines.

Ten days to two weeks after FECV infection, titer raises. No fever. Dr. Pedersen wants us to stop saying "feline coronavirus" and instead say "feline enteric coronavirus". Virus is shed at extremeely high levels in feces. Fecal to oral transmission. Litterpans contaminate environment efficiency. Shedding varies, some cats are non-shedders (shed for a little bit, then immune), some are chronic shedders (never clear virus). Most cats cycle through shedding, clearing and reinfection.

Used to be thought could prevent infection with early weaning. Not true, kittens start shedding before three weeks of age, they just don't have a titer until maternal immunity wanes. Not practical for catteries to keep FECV out.

Looked at shelter situations. Sacramento county animal control. No cats less than eight weeks of age were infected with FECV. All from 8-56 week olds were. Only half of cats over 56 weeks of age were infected. The virus is everywhere. Shedding: 100 virus particles per grain-of-wheat sized particle of feces up to 100 MILLION virus particles!

One week post primary exposure in kittens lead to heavy shedding. Shedding in adult cats increased after entry into shelter. Stress increaases infectivity. More virus may mean more mutation episodes.

In nature, where litters are more isolated than in catteries, kittens are infected later. Kittens shedd 100-fold more virus than adults.

Experimental FIP is 70-100% fatal. Disease signs appear when antibodies develop. Antibodies not protective, but case worse disease. FIPV not found outside of the body. 10-12 days after FIPV infection, fever and antibodies develop.

Weight loss, spiking fevers, and peritoneal effusion is "wet FIP". Dry FIP shows as uveitis, isolated, localized disease. Immune response almost worked. Now see more dry FIP than wet FIP. FIP was not reported before about 1955, corresponding with people starting to keep litterboxes and cats inside. May be evolutionarily developing into more resistence (more dry FIP than wet).

Risk factors: age (6-18 months)j catteries, shelters, other high density environment; genetic predisposition. Don't use males that have thrown FIP. Not sex-linked to males, but if males are controlled, females don't have to be as much... Not as influential genetically.

Incidnece of FIP in catteries comes and goes. Epidemic one year may suddenly go away the next year. Depopulation useless, just stay the course. Do different breedings, wait for a "hot strain" to die out? STAY CALM in the face of FIP. Don't overreact.

Antibody response correlated with fecal shedding. Fecal shedding very erratic. Some cats shed for a while and seem to never shed again. Single point titers inaccurate and meaningless. Recovery is usually associated with a drop in titer. Titers over 1:100 or 1:400 usually associated with shedding. But these numbers fluctuate. Be careful with interpretation.

Genetics: different cats respond to infection differently. Probably a genetic influence. Genetics of the immune system VERY complex. Creating two colonies of cats: highly resistent and highly susceptible. Vaccines worthless, no drugs treat this, genetics are the only real hope.

Cytokine response in vaccinated cats exposed to FIP was different. Immunity to FIP is cell mediated. Vaccine was worthless, but observed that surviving cats had high interferon gamma response and no tumor necrosis factor response, but FIP cats had no IFN-g response but a high TNF response. Mice with IFN-g gene knocked out die of a FIP like disease following coronavirus exposure. IFN is a marker for a broader immune reaction.

Selective breeding is happening naturally for FIP resistance. Seems to be less FIP than there used to be. **No effective vaccine will ever exist for FECV** If a cat can't wage an adequate immune response to the native virus, it can't form an effective immune response to the vaccine strain either.

There is now a shelter medicine program at UC Davis. Lots to learn on implications of the effect of husbandry on overall cattery health... It isn't all genetics!

Use of interferon is an expensive placebo in his opinion. In catteries, don't get involved in getting titers. You'll spend thousands of dollars for a bunch of meaningless numbers. Definitive test is immunohistology of macrophages, but FIP really not a difficult disease to diagnosis if you look at the whole picture.

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