Updated: Feb 3, 2021
What is Feline infectious peritonitis (FIP)?
Feline infectious peritonitis (FIP) is an immune-mediated disease triggered by infection with a feline coronavirus (FCoV). Coronavirus-specific antibodies are present in the majority of cats. However, <5% of FCoV-infected cats develop FIP in multicat households. , 
Where is FIP Virus found in nature?
FCoV infection and FIP occur worldwide with similar prevalence and are found in both domestic and wild cats. There are two strains of FCoV, FCoV serotype I and FCoV serotype II. These subtypes are dependent on their relationship to canine coronavirus (CCoV) antigenically, and their proportions vary in different countries. Most cats with FIP have been infected with FCoV serotype I. However, both serotypes can cause FIP, and both can cause clinically inapparent FCoV infections.
FCoV belongs to the same cluster of coronaviruses found in pigs, dogs, and humans coronaviruses. Coronaviruses have a relatively restricted organ preference, mainly infecting the respiratory and/or gastrointestinal tracts. In cats, however, coronavirus infections can, in certain circumstances, involve multiple organs.
How does a cat get (FIP) virus?
FIP is a sporadic disease caused by viral variations that develop within each specific cat. The pathogenesis (development) of FIP is unclear, but there are two main theories.
The “internal mutation theory."
This theory states that cats are infected with the primarily less potent Feline Coronavirus (FCoV) that reproduces in cells within the intestines. A change then occurs in a certain region of the FCoV genome that creates a new phenotype with the ability to replicate within other cells called macrophages. Viral reproduction in macrophages is the defining event in FIP, a critical contributing factor for the development of FIP. Macrophages replicate the mutated coronavirus and carry it to target tissues such as the abdominal cavity, thorax, kidneys, eyes, and the nervous system, resulting in widespread immune-mediated inflammation of blood vessels. .
The existence of distinct circulating virulent and avirulent strains in a population, and exposure to the pathogenic strain theory
The viral load and the cat’s immune response determine whether FIP will develop. It is likely both viral genetics and host immunity play a role.
In both theories, the key infective event in the development of FIP is the massive replication of FCoV in macrophages. If the cat does not eliminate macrophages infected with replication-competent virus early in the infection, the presence of the virus within circulating macrophages initiates an ultimately fatal immune-mediated reaction, which defines FIP.
What factors contribute to the development of FIP in cats?
Factors that increase FCoV replication in the intestines (and increase the probability of the mutation) include:-
■ Young age,
■ Breed predisposition,
■ Immune status,
■ Corticosteroid treatment,
■ Dosage and virulence of the virus and
■ Reinfection rate in multicat households.
■ Crowded environments, such as catteries or shelters, also may increase stress and exposure to FCoV.
Whenever FCoV infection exists, so does the potential for the development of FIP.
How is FIP transmitted?
FCoV and FIP are a major problem in multicat households where many cats are kept together in a confined space (e.g., catteries, shelters, pet stores). FCoV is found less commonly in free-roaming community cats because they do not typically use the same locations to bury their faeces; shared litter boxes are a significant source of transmission in multicat households.
A cat becomes infected with FCoV via a faecal-oral transmission (or less commonly, inhalation). The main site of viral multiplication is the intestinal lining. Replication of FCoV in the intestinal cells leads to diarrhoea in some cats. In many cats, the infection persists for weeks to months in the absence of clinical signs. These cats shed FCoV either intermittently or continually and act as a source of infection for other cats. FIP is a complex immune disease involving viral antigen, antiviral antibodies, and complement. Within weeks after macrophage invasion and replication, virions are found in the cecum, colon, intestinal lymph nodes, spleen, and liver after distribution by macrophages in the whole body, including the CNS.
Most commonly, kittens are infected at the age of 6–8 wk at a time when their maternal antibodies wane, mostly through contact with faeces from their mothers or other FCoV-excreting cats.
FCoV is a relatively fragile virus that is destroyed by most household disinfectants and detergents. However, it may survive in cold or dry conditions (e.g., in carpet) for as long as 7 wk outside the cat. Indirect fomite transmission is possible, and the virus can be transmitted for a short time via clothes, toys, and grooming tools.
What are the clinical signs of FIP?
■ Progressive distention of the abdomen due to fluid buildup
■ Lung involvement and difficulty breathing
■ Fever lasting 2 to 5 weeks
■ Loss of appetite
■ Weight loss
■ History of vague illness, including longterm fever, malaise, weight loss, and occasionally major organ system failure (kidneys, liver)
■ Eye and central nervous system signs may occur simultaneously or independently.
■ About 50% of all cats have signs related to the involvement of abdominal organs (kidney, liver, spleen, pancreas, lymph nodes)
NB: Reproductive disorders, neonatal deaths, and fading kittens are not usually associated with FIP.
How is FIP Treated?
Treatment of cats with FIP remains frustrating and is limited to the cases that respond favourably within the first few days. The prognosis for a cat with FIP is very poor. Cats that show no improvement within 3 days after treatment initiation are unlikely to show any benefit from therapy and euthanasia should be considered. Longer survival or remission from clinical signs is rare.
Supportive treatment is aimed at suppressing the immune overreaction, usually using corticosteroids. Cats treated with corticosteroids have shown anecdotal improvement for as long as several months. Immunosuppressive drugs such as prednisolone (2–4 mg/kg/day, PO) are commonly used. Itraconazole (5-10 mg/kg PO SID), though used for fungal infections in cats, it exhibits antiviral effect in cells after a viral infection, signifying that itraconazole could potentially be used as a therapeutic. 
Cats with FIP should receive supportive therapy, including fluids and nutritional support, and their quality of life should be monitored.
How are exposed cats managed?
■ When a cat in a household develops FIP, all in-contact cats will have already been exposed to the same FCoV. However, it is not recommended to allow contact between a cat with FIP and any new “naive” cat. Kittens, which are more susceptible to FIP than adults, should not be introduced to households with a recent history of FIP.
■ If a cat has been euthanized or has died due to FIP, the owner should wait for 2 months before obtaining another cat. FCoV can remain infectious for at least 7 wk in the environment, particularly where litter boxes are in use. Other cats currently in the household are most likely infected with and shedding FCoV.
■ Although exposed cats will most likely have antibodies, this is not necessarily associated with a poor prognosis. Most cats infected with FCoV will not develop FIP, and many cats in single- or two-cat households will eventually clear the infection and become antibody negative in a few months to years (usually ~6 mo).
How are Multicat Households Managed?
■ In most multi-cat households with unusually high cat numbers, FCoV is endemic, and FIP is almost inevitable. Households of <5 cats may spontaneously and naturally become FCoV-free, but in households of >10 cats per group, this is almost impossible because the virus passes from one cat to another, maintaining the infection. In these FCoV-endemic environments, such as breeding catteries, shelters, foster homes, and other multicat homes, there is virtually nothing to prevent FIP.
■ Reducing the number of cats (especially of kittens <12 mo old) and keeping suspected FCoV-contaminated surfaces clean can minimize population loads of the virus.
■ The antibody or faecal PCR testing and removal of positive cats should be performed to stop exposure and reinfection of recovered cats.
■ An early weaning protocol for prevention of FCoV infection in kittens is encouraged. It consists of isolation of queens 2 wk before parturition, strict quarantine of queen and kittens, and early weaning at 5 wk of age. Kittens should be taken to a new home (with no FCoV-infected cats) at 5 wk of age.
■ Another possible approach is to maximize heritable resistance to FIP in breeding catteries. Genetic predisposition plays a role in the disease but is not completely understood. Full-sibling littermates of kittens with FIP have a higher likelihood of developing FIP than other cats in the same environment. A cat that has two or more litters in which kittens develop FIP should not be bred again.
■ In shelters, prevention of FIP is virtually impossible unless cats are strictly separated and handled only through sterile handling devices (comparable to isolation units). Isolation is often not effective because FCoV is easily transported on clothes, shoes, dust, and cats.
■ Personnel should understand that FCoV is an unavoidable consequence of endemic FCoV in multi-cat environments. Good husbandry practices and facilities that can be cleaned easily may minimize virus spread.
Is there a risk of transmission of FIP to humans?
Although coronaviruses are shared with animals, such as the severe acute respiratory syndrome (SARS) and the Middle East respiratory syndrome (MERS), are responsible for severe respiratory disease outbreaks in people, there is no indication that FCoV is infectious to people.
 L. D. Pesteanu-Somogyi, C. Radzai and B. M. Pressler, “Prevalence of feline infectious peritonitis in specific cat breeds.,” Journal of feline medicine and surgery, vol. 8, no. 1, pp. 1-5, 2006.
 N. C. Pedersen, J. F. Boyle, K. Floyd, A. Fudge and J. Barker, “An enteric coronavirus infection of cats and its relationship to feline infectious peritonitis.,” American Journal of Veterinary Research., vol. 42, no. 3, pp. 368-377, March 1981.
 K. Shirato, H. W. Chang and P. J. M. Rottier, “Differential susceptibility of macrophages to serotype II feline coronaviruses correlates with differences in the viral spike protein.,” Virus Research, vol. 255, pp. 14-23, 15 Aug 2018.
 S. Birchard and R. Sherding, “Feline Infectious Peritonitis (Feline Coronavirus),” in Saunders Manual of Small Animal Practice, 3rd ed., Saunders, 2006.
 F. Riemer, K. A. Kuehner, S. Ritz, C. Sauter-Louis and K. Hartmann, “Clinical and laboratory features of cats with feline infectious peritonitis--a retrospective study of 231 confirmed cases (2000-2010).,” Journal of Feline Medicine & Surgery, vol. 18, no. 4, pp. 348-56, April 2016.
 T. Ishida, A. Shibanai, S. Tanaka, K. Uchida and M. Mochizuki, “Use of recombinant feline interferon and glucocorticoid in the treatment of feline infectious peritonitis.,” Journal of Feline Medicine & Surgery, vol. 6, no. 2, pp. 107-9, April 2004.
 T. Takano, M. Akiyama, T. Doki and T. Hohdatsu, “Antiviral activity of itraconazole against type I feline coronavirus infection.,” Veterinary Research, vol. 50, no. 1, 18 Jan 2019.
The Advisory Board on Cat Diseases website: www.abcdcatsvets.org/feline-infectious-peritonitis/