Introduction

• Infectious disease with an immune-mediated component.
• Cause: feline coronavirus (FCoV)  Feline coronavirus: FIP.
• Signs: occurs in two forms, effusive (wet) and non-effusive (dry): 
  • Effusive form: major clinical signs include ascites, dyspnea, fever, anorexia and wasting.
  • Non-effusive form: major clinical findings include neurological signs, fever, renal and hepatic failure, uveitis, anorexia and wasting.
  • On post-mortem examination mixed forms are commonly seen.
• Diagnosis: signalment, history, signs, clinical pathology findings can raise suspicion. Histopathology combined with immunostaining for FCoV is only reference diagnostic method. Seropositivity for FCoV does not confirm a diagnosis of FIP as most seropositive cats are healthy and will not develop FIP.
• Treatment: spportive; antiviral agents, immunosuppression, immunomodulation.
• Prognosis: hopeless in long-term. A few cats can maintain a reasonable quality of life for some weeks, rarely months.
  Print off the owner factsheet on FIP Feline Infectious Peritonitis (FIP) to give to your client.

Pathogenesis

Etiology

• FCoV is an enveloped, single-stranded, positive-sense RNA coronavirus:
  • Can infect domestic and wild felids.
  • High rate of genetic mutation.
• FIP is a sequela of FCoV infection in some cats.
• Two serotypes of FCoV exist:
  • FCoV serotype I is considered wholly feline.
  • FCoV serotype II is thought have arisen from recombination events between serotype 1 FCoVs and canine coronavirus.
  • Both serotypes have been associated with FIP.
  • Prevalence of each serotype appears to vary from country to country, with serotype I most prevalent in Europe.

Predisposing factors

• Exposure to FCoV is more likely in cats from rescue shelters, breeding colonies, and show cats.
• History of recent stressor noted in over half of cats developing FIP:
  • Adoption.
  • Vaccination.
  • Elective surgery (eg neutering).
  • Boarding in cattery, breeding, spending time in an animal shelter.
  • Respiratory tract disease.
  • In-contact cat developing FIP.
  • Introduction of a new cat.

Pathophysiology

• Disease is dependent upon the interaction of FCoV with the individual’s immune system, therefore not all cats which are infected with FIP will develop FIP. The large majority of cats infected with FCoV seroconvert but show no clinical signs. In most situations less than 5% of FCoV serology-positive cats go on to develop FIP.

Transmission of FCoV

• FCoV shed in feces – litter trays, contaminated fomites, contaminated coat are potential sources of infection.
• FCoV shed in saliva.
• Transplacental transmission very rare.

Pathogenesis

In most cats

• Oronasal infection with FCoV → replication in intestinal epithelial cells:
  • May cause mild enteric +/- respiratory signs.
  • Shedding of FCoV in feces from 2 days and may continue for several months (+/- intermittently thereafter).
  • Intestinal macrophages uptake FCoV → regional lymph nodes → monocyte associated viremia.
• 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, the host immune response eventually eliminates FCoV. A small number may become long-term carriers.

In a small number of cats

• FCoV mutates within the macrophages / monocytes → enhanced cell tropism and replication → immune-mediated response → vasculitis / granuloma formation.
• The mutations which produce a virus capable of causing FIP are not the same in each cat, and at least two viral genes are involved.
• Mutations in the fusion peptide of the spike protein of serotype 1 FCoVs have been implicated in monocyte/macrophage tropism by affecting fusogenic activity and cell receptor specificity:
  • Most cats with FIP have one of these mutations in FCoV from affected tissues.
  • Cats without FIP do not have these mutations in FCoV found in their feces.
  • These mutations have been reported with high frequency in FCoV found in tissues from cats without FIP.
• Mutations in the furin cleavage motif and the heptad HR1 region of the S2 subunit of the spike protein have also been correlated with disease.
• Truncations of the accessory protein 3c gene have been associated with loss of ability to replicate within enterocytes and have only been reported with FIP-associated FCoVs; however, complete accessory protein 3c genes are also seen in FIP-associated FCoVs in 30-40% of affected tissues.
• Although mutated FCoV may be shed in feces, it is unclear whether these strains are infective to other cats.

Timecourse

• Incubation period following experimental infection is 2-14 days for effusive disease and several weeks for non-effusive disease.
• Incubation period following natural exposure is 6 weeks in specific-pathogen-free cats.

Epidemiology

• Most cats are first exposed and infected with FCoV as kittens by other cats in a household.
• Some cats are presumably infected with FCoV when they enter an endemically-infected household.
• A few cats may be carriers for prolonged periods of time; FCoV shedding may increase at times of stress.
• Not all endemically-infected households have cases of FIP.

Diagnosis

Treatment

Prevention

Outcomes