Update on feline infectious peritonitis (Proceedings)


Update on feline infectious peritonitis (Proceedings)

Apr 01, 2008

Despite improvements in our understanding of the pathogenesis of FIP, FIP remains a leading cause of death in young cats, especially purebred catteries, shelters.

The virus that causes FIP, feline coronavirus, is an enveloped RNA virus. Feline coronaviruses are divided into two groups:

  • Highly pathogenic, feline infectious peritonitis viruses (FIPV)
  • Feline enteric coronaviruses, which generally cause mild enteritis (FECV).

There viruses CANNOT as yet be distinguished from one another.

Feline coronaviruses mutate readily and it is now accepted that FECV eventually mutates to form virulent FIPV. Mutation occurs soon after infection with FECV, or years later.


Seroprevalence of feline coronavirus is 25% in single cat households and 75% to 100% in multicat households. Mortality rate in single/two cat households is 1/5000, in catteries it can reach 5%. Rarely, epidemics of FIP occur in catteries.

The incidence of FIP is related to levels of virus in the environment, virus factors and host factors. Immunosuppression resulting from overcrowding and stress and genetic factors are important. Purebred cats are more susceptible, cats are usually aged 3 months to 3 years; occasionally they are > 10 years, presumably due to poor immune function. Maternal antibody wanes at about 6 weeks of age.


Spread of FcoV is FECAL-ORAL, and the virus is very infectious. Some strains remain infective for weeks at room temperature. Most cats shed intermittently, with cycles of recovery and reinfection. Some shed chronically; these cats are important in maintaining the incidence of FIP


FECV replicates in enterocytes and destroys the villus tips, with sometimes mild fever, small bowel diarrhea, and vomiting. FECV eventually mutates to virulent FIPV, which is able to multiply in MACROPHAGES!! Infected monocytes deposit in the endothelial lining of small venules. With a strong cell-mediated immune (CMI) response, the virus is eliminated or latent infection occurs. Stress can reactivate the infection, with development of fulminant FIP.

If CMI is not mounted, PYOGRANULOMATOUS VASCULITIS results due to deposition antigen-antibody complexes in the venular endothelium. Pleural and peritoneal effusion develop (= EFFUSIVE FORM). With partial CMI, viral replication slows ® granuloma formation (= NONEFFUSIVE FORM). This may deteriorate to wet FIP if the CMI response wanes.

ANTIBODY-DEPENDENT DISEASE ENHANCEMENT (ADDE) is the term referring to acceleration of disease by the humoral immune response. Antibodies bind to Fc receptors on macrophages with more rapid viral replication and dissemination. This has implications for vaccination. Production of antibodies is essential for disease to occur, as FIP is an immune-complex disease.


Antemortem diagnosis of FIP is like completing a jigsaw puzzle. It is the combination of abnormalities that is often useful. Clinicopathologic findings include:

  • CBC: nonregenerative anemia; neutrophilia, lymphopenia.
  • Serum chemistry and urinalysis:
  • Proteinuria, azotemia.
  • Elevated liver enzymes, coagulopathies
  • Many (but not all) cases have hyperproteinemia
  • In cats with neuro signs, CSF may show hyperproteinemia and increased neutrophils and lymphocytes (but usually it does not).
  • Effusion fluid: sometimes (but not always) it is high protein (5 to 12 g/dL), thick and tenacious (an EXUDATE). Clear to yellow, may contain fibrin clots. Cellularity is low. Predominant cells are neutrophils (also may see mononuclear cells). Rivalta's test can help differentiate exudates from transudates, but is still not specific for FIP in any one cat.