Felis ISSN 2398-2950

Feline coronavirus: FIP

Synonym(s): Feline coronavirus, FCoV, feline infectious peritonitis, FIP, feline enteric coronavirus, FECV, feline infectious peritonitis virus

Contributor(s): Diane Addie, Susan Dawson, Danielle Gunn-Moore, Melissa Kennedy, Emi Barker

Introduction

Classification

Taxonomy

  • Family: Coronaviruses.

Etymology

  • Corona is Latin for crown.
  • The coronavirus has a halo of peplomer (glycoprotein spikes) visible on electron microscopy.

Active Forms

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Clinical Effects

Epidemiology

Habitat

  • Epithelial cells of the small and large intestine.
  • Monocytes/macrophages.

Transmission

  • Shed in the feces and occasionally the saliva.
  • Direct, by cat-to-cat contact, eg nose to nose, mutual grooming and contaminated coat.
  • Indirect, especially using shared litter trays, but also via contaminated fomites.
  • Transplacental transmission extremely rare.

Pathological effects

  • FCoV is ingested or possibly inhaled.
  • Oronasal infection with FCoV → replication in intestinal epithelial cells (and possibly within the oropharynx):
    • 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.
  • In most cats mucosal immunity (IgA) and possibly cell-mediated immunity develops and infection ceases. A small number may become long-term carriers.
  • Some cats exhibit severe diarrhea which may be refractory to treatment and last for months. Some have diarrhea and third eyelid syndrome.
  • Effectiveness of cat's cell-mediated immune (CMI) response correlates with disease: good CMI → clear virus, poor CMI → disease.
  • In a small number of cats (<10%) FCoV mutates within the macrophages/monocytes → enhanced cell tropism and replication → immune-mediated response → vasculitis/granuloma formation.
  • Cats generally have elevated levels of immunoglobulins, reducing the albumin:globulin ratio to <0.6.
  • Cats with clinical FIP generally have very high anti-FCoV antibody titers. However, many clinically healthy cats have high titers, and some cats with FIP may test negative for antibody (possibly due to high antigen concentration binding the antibody, preventing its detection by the assay. 
  • 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 I 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 erythrocytes 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.

Control

Control via chemotherapies

  • No treatment currently known to stop FCoV shedding of carrier / transiently infected cats.
  • Cats with FCoV-associated diarrhea are treated symptomatically.
  • For treatment of cats with FIP see Feline infectious peritonitis.

Control via environment

  • Control of FCoV infection is based on reducing environmental viral levels by reducing factors that increase viral load and shedding by individuals, and clearing of virus from the environment:
    • Reducing the number of cats kept in any small area.
    • Avoiding the introduction of FCoV-infected cats to naïve cats.
    • Avoiding introducing FCoV to uninfected cats via contaminated bowls, litter trays, cages, etc.
    • Good hygiene as feces is major source of virus, remove feces from litter trays as soon as possible after use and regularly disinfect trays using sodium hypochlorite.
    • Keeping cats in good health.
    • Reducing stress on cats.
  • For control of FCoV under specific circumstances (eg breeding cattery) see Feline infectious peritonitis.

Vaccination

  • A vaccine is available in the USA and in parts of mainland Europe, but is not recommended by consensus panels of American or European Feline Specialists.
  • This vaccine is a temperature-sensitive, serotype 2, mutant FCoV which is administered intra-nasally.
  • The vaccine is reported to be safe and has efficacy of approx. 50-75% as a preventable fraction.
  • However, it will not prevent disease after exposure to FCoV and, where licensed, is administered at >16 weeks of age at which time many kittens will have been infected.

Diagnosis

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Further Reading

Publications

Refereed papers

  • Recent references from VetMed Resource and PubMed.
  • Takano T, Akiyama M, Doki T, Hohdatsu T (2019) Antiviral activity of itraconazole against type I feline coronavirus infection. Vet Res 50(1), 5 PubMed.
  • Shirato K, Chang H W, Rottier P J M (2018) Differential susceptibility of macrophages to serotype II feline coronaviruses correlates with differences in the viral spike protein. Virus Res 255, 14-23 PubMed.
  • Tasker S (2018) Diagnosis of feline infectious peritonitis: Update on evidence supporting available tests. J Feline Med Surg 20, 228-243 PubMed.
  • Barker E N, Stranieri A, Helps C R, Porter E L, Davidson A D, Day M J et al (2017) Limitations of using feline coronavirus spike protein gene mutations to diagnose feline infectious peritonitis. Vet Res 48, 60.
  • Riemer F, Kuehner K A, Ritz S, Sauter-Louis C, Hartmann K (2016) Clinical and laboratory features of cats with feline infectious peritonitis - a retrospective study of 231 confirmed cases (2000-2010). J Feline Med Surg 18, 348-356 PubMed.
  • Borschensky C M, Reinacher M (2014) Mutations in the 3c and 7b genes of feline coronavirus in spontaneously affected FIP cats. Res Vet Sci 97, 333-340 PubMed.
  • Kipar A, Meli M L (2014) Feline infectious peritonitis: still an enigma? Vet Pathol 51, 505-526 PubMed.
  • Golovko L, Lyons LA, Liu H, Sorensen A, Wehnert S, Pedersen N C (2013) Genetic susceptibility to feline infectious peritonitis in Birman cats. Virus Res 175, 58-63 PubMed.
  • Chang H W, Egberink H F, Halpin R, Spiro D J, Rottier P J (2012) Spike protein fusion peptide and feline coronavirus virulence. Emerg Inf Dis 18, 1089-1095 PubMed.
  • Addie A, Belak S, Boucraut-Baralon C, Egerink H, Frymus T, Gruffydd-Jones T, Hartmann K, Hosie M J, Lloret A, Lutz H, Marsilio F, Pennisi M G, Radford A D, Thiry E, Truyen U, Horzinek M C (2009) Feline infectious peritonitis ABCD guidelines on prevention and management. J Feline Med Surg 11(7), 594-604 PubMed.
  • Regan A D, Shraybman R, Cohen R D, Whittaker G R (2008) Differential role for low pH and cathepsin-mediated cleavage of the viral spike protein during entry of serotype II feline coronaviruses. Vet Micro 132, 235-248 PubMed.

Other sources of information

Organization(s)

  • International Society of Feline Medicine (ISFM) (formerly the European Society of Feline Medicine) Place Farm, Tisbury, Wiltshire, SP3 6LW, UK. Tel: + 44 1747 871872; E-mail: info@icatcare.org
  • Feline Virus Unit, Department of Veterinary Pathology, University of Glasgow, Bearsden Road, Glasgow G61 1QH, Scotland. Tel: + 44 141 330 5777; Fax: + 44 141 330 5748; E-mail: vet-sch-vds@glasgow.ac.uk.
  • Bristol Vet School, Bristol University, Langford House, Langford, Bristol, BS18 7DU. labs@langfordvets.co.uk

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