Felis ISSN 2398-2950

Feline infectious peritonitis

Synonym(s): FIP

Contributor(s): Diane Addie, Stephen Barr, Nicki Reed, Kim Willoughby


  • Infectious disease with an immune mediated component.
  • Cause: feline coronavirus Feline corona virus: FIP.
  • Signs: occurs in two forms, wet (effusive) and dry (non-effusive):
    • Wet form: major clinical signs include ascites, dyspnea, pyrexia, anorexia and wasting.
    • Dry form: major clinical findings include neurological signs, pyrexia, renal and hepatic failure, uveitis, anorexia and wasting.
  • Diagnosis: signalment, history, signs, clinical pathology findings can raise suspicion. Histopathology is only definitive method.
    Serology - seropositivity for feline coronavirus does not confirm a diagnosis of FIP. Most seropositive cats are healthy and will not develop FIP.
  • Treatment: supportive.
  • Prognosis: hopeless in long term. A few cats can maintain a reasonable quality of life for some weeks.
    Print off the owner factsheet on FIP Feline Infectious Peritonitis (FIP) to give to your client.



  • Feline coronavirus.
  • Two subtypes of FCoV exist: FCoV serotype I is considered wholly feline, whereas FCoV serotype II is thought to have arisen from mutation between canine coronavirus and FCoV type I. Both serotypes have been associated with the disease of FIP, and the prevalence of each appears to vary from country to country, with serotype I being most prevalent in Europe.
  • The concept of 'enteric' and 'FIP-inducing' strains is probably redundant, as recent work has demonstrated that the previously called 'FIP-inducing' strains of feline coronavirus arise from mutation of feline coronavirus within individual cats. The mutations which produce a virus capable of causing FIP are not the same in each cat, and at least two virus genes are involved.

Predisposing factors


  • Cat from multi-cat household.
  • Cat acquired from multi-cat household within previous few months.
  • History of recent stressor (eg show, visit to stud, elective surgery).
  • In studies conducted in the UK, the prevalence of antibodies to coronaviruses has been reported to be 22.4% in stray cats (Muirden, 2002), 53% in breeding colonies and 82% of show cats (Sparkeset al, 1992). The prevalence of FIP is markedly less than the prevalence of coronavirus infection, with only approximately 10% of FCoV positive cats within multi-cat households developing FIP.


As disease is dependant upon the interaction of the virus with the immune system, not all cats which are infected develop clinical disease. The large majority of infected cats seroconvert and show no clinical signs.

Basic pathogenesis where FIP develops

  • Oronasal infection   →   replication in intestinal epithelium   →   broad dissemination to many tissues via macrophages   →   immune mediated response   →   granuloma formation   →   disease dependant upon site of granulomata formation.


  • Though the main site of replication is the gut, virus can also be detected in tonsil and upper respiratory tract early in infection.
  • Virus is shed in saliva and feces. Fecal shedding can occur from 2 days post infection and may continue for several months. Cats that continue to shed for more than 10 months may be considered chronic carriers.
    The risk of shedding virus and the amount of virus shed relates to antibody levels: cats with higher antibody titers shed more virus and antibody negative cats are unlikely to shed virus.
  • In the majority of cats, infection does not result in disease but does result in an immune response which eventually eliminates the virus. A very few cats may become long-term carriers.
  • There are two main theories to explain granuloma formation in affected cats
    Either Virus in tissue attracts antibodies and complement, causing migration of more macrophages and neutrophils to form granuloma. This theory gave rise to the concept that; good cell mediated immunity (CMI)   →   no disease, partial CMI   →   non-effusive FIP and that poor CMI   →   effusive FIP.
    Or Circulating immune complexes attach to blood vessel walls, attracting complement and inducing granulomata formation as above. The immune complexes then fix complement and inflammatory mediators are released causing vasculitis and leakage of plasma proteins. This second theory is attractive due to the distribution of lesions, which suggests an immune complex mediated disease.
  • The reason why some cats infected with FCoV develop FIV and others do not is incompletely understood. The virus may undergo a mutation, with deletion of part of the genome, resulting in it becoming more virulent and thus able to replicate within macrophages. The immune response by the individual cat is also a factor, with young or immunosuppressed individuals being more likely to develop disease. Cats with a strong humoral response (ie antibody formation) may be more prone to developing FIP, whereas those with a strong cell mediated immune response appear resistant.


  • The incubation period may be prolonged. Cats may be long term carriers of the virus and, in cases where disease occurs the virus is thought to mutate within the cat to a pathogenic form for that animal.


  • Most cats are infected as kittens by other cats in a household.
  • Some cats are presumably infected when they enter an endemically infected household.
  • A few cats may be carriers for prolonged periods of time.
  • Not all infected households demonstrate clinical evidence of infection (ie FIP).


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Further Reading

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