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Feline calicivirus

Professor Alan Radford examines the epidemiology, clinical signs, diagnosis and treatment of feline calicivirus (FCV), a small, non-enveloped, single-stranded ribonucleic acid (RNA) virus, mainly shed in ocular, nasal and oral secretions.

Feline calicivirus is a member of the calicivirus family. As with many RNA viruses, FCV can evolve quickly and this creates clinical variation that can be challenging for diagnosis and control. Strains of FCV vary slightly in pathogenicity and antigenicity, although they are all sufficiently cross-reactive to be classified as one serotype, making vaccine protection a reality. This genetic diversity is useful epidemiologically as it allows tracking of infection.

Epidemiology

FCV infections are fairly widespread in the general cat population, with highest prevalence in multi-cat households, shelters and in younger animals. The virus is mainly shed in ocular, nasal and oral secretions, with spread largely by direct contact with an infected cat. However, contaminated secretions can be infectious for several days on cages, feeding, cleaning utensils and personnel.

As well as acutely infected cats, clinically recovered “carriers” can also transmit infection, some for many months. Such carriers are widespread in the population and are probably the main reason why FCV is so successful. Approximately 10% of household cats and 25% to 75% of shelter or colony cats test positive for FCV. Although the precise mechanism of persistence is unclear, it is likely to include evolution of the viral capsid protein allowing the virus to escape the host's immune response. Longitudinal studies of endemically infected colonies have shown that, although many cats appear to be long-term carriers, only a small minority (approximately 10%) are truly persistently infected, the remainder undergoing cycles of reinfection.

Clinical signs

Strains of FCV can differ in tropism and virulence and a wide range of clinical signs may be seen. Most strains induce a fairly characteristic, mild syndrome characterised by pyrexia, oral ulceration, and mild respiratory and conjunctival signs. Other FCV isolates produce a febrile self-limiting disease of shifting lameness and pyrexia, with or without oral and respiratory signs. Some strains of FCV however are non-pathogenic whilst others are more virulent. Rarely, kittens may develop a fatal pneumonia.

Several outbreaks of a severe virulent systemic disease (FCV-VSD) with high mortality have been described, particularly in the United States and Europe. Cats with FCV-VSD variably show:

  • Facial and paw oedema
  • Pyrexia
  • Classic signs of oral ulceration and upper respiratory infection
  • Icterus
  • Hemorrhages from the nose and in the faeces.

Mortality can be high. Some of the outbreaks are nosocomial, and each appears to have been caused by a different FCV strain. Although highly contagious within a group of cats, all outbreaks appear to have been contained, and the disease has not spread into the general population.

Feline chronic gingivostomatitis is a frustrating and extremely challenging condition to treat that is strongly associated with FCV infection. We use the phrase “associated with” because the disease has not been recreated experimentally suggesting other host and microbial factors are likely to be involved. The prevalence of this condition has been estimated at 0.7% of consultations in first opinion practice in the UK.

Diagnosis

While clinical signs can be highly suggestive of FCV, they are rarely pathognomonic. Although specific diagnostic testing is not always necessary, identifying a causative agent may be helpful when disease is severe, warranting specific therapy. This is where multiple cats are involved and where disease occurs in vaccinated cats.

Diagnosis of FCV is generally made using oropharyngeal swabs and either viral isolation or reverse transcriptase polymerase chain reaction. Due to carriers, a positive test does not prove FCV was the cause of any clinical signs.

Treatment

There are no published antiviral therapies for acute FCV infection. Some authors advocate the use of Interferon to treat feline chronic gingivostomatitis complex although to the authors knowledge this lacks proven efficacy. In most cases of viral respiratory disease, antibacterial treatment is not indicated. In severe cases, broad-spectrum antibacterials that achieve good penetration into the respiratory tract may help control secondary bacterial infection.

Find out more about responsible antibacterial use in the veterinary community.

Vaccination

Vaccination is licensed to reduce clinical signs of acute upper respiratory tract disease and has been the mainstay of FCV control for many years.

  • Although different vaccine companies use different FCV strains, it is generally considered that all licensed vaccines offer broadly similar levels of protection and there is no evidence for a decline in protection over time
  • Vaccination does not protect against infection or cats becoming carriers
  • FCV diversity means vaccines may vary in the degree of protection they offer to individual strains
  • The effect of vaccines on chronic stomatitis is not known and they are not licensed for its control
  • For FCV-VSD, it is clear that many outbreaks have been reported in vaccinated animals. Whether other potentially virulent strains exist in the field, but remain undetected because they are neutralised by vaccination, is not known.

For routine vaccination programs, all types of vaccine appear to be suitable. The American Association of Feline Practitioners (AAFP), the Advisory Board on Cat Diseases (ABCD), and the World Small Animal Veterinary Association (WSAVA) all recommend every cat is vaccinated against FCV at nine and 12 weeks, followed by a one-year booster. Some recommend an additional kitten vaccine at 16 weeks. Most now recommend cats are subsequently vaccinated every three years although ABCD still recommends that cats at high risk are vaccinated annually.

References

Guidelines

  • Day MJ, Horzinek MC, Schultz RD. 2010. Guidelines for the vaccination of dogs and cats. Compiled by the Vaccination Guidelines Group (VGG) of the World Small Animal Veterinary Association (WSAVA). J Small Anim Pract 51:338-356
  • Hofmann-Lehmann R, Hosie MJ, Hartmann K, Egberink H, Truyen U, Tasker S, Belák S, Boucraut-Baralon C, Frymus T, Lloret A, Marsilio F, Pennisi MG, Addie DD, Lutz H, Thiry E, Radford AD, Möstl K. Calicivirus infection in cats. Viruses. 2022 Apr 29;14(5):937. doi: 10.3390/v14050937
  • Richards JR, Elston TH, Ford RB, et al. 2006. The 2006 American Association of Feline Practitioners Feline Vaccine Advisory Panel report. J Am Vet Med Assoc 229:1405-1441.

Vaccines

  • Addie D, Poulet H, Golder MC. 2008. Ability of antibodies to two new caliciviral vaccine strains to neutralise feline calicivirus isolates from the UK. Veterinary Record 163:355-557
  • Smith SL, Afonso MM, Pinchbeck GL, Gaskell RM, Dawson S, Radford AD (2019). Temporally separated feline calicivirus isolates do not cluster phylogenetically and are similarly neutralised by high-titre vaccine strain FCV-F9 antisera in vitro. Feline Med Surg.. doi: 10.1177/1098612X19866521. This is an e-publication
  • Poulet H, Brunet S, Leroy V, et al. 2005. Immunisation with a combination of two complementary feline calicivirus strains induces a broad cross-protection against heterologous challenges. Veterinary Microbiology 106:17-31
  • TerWee T, Lauritzen A, Sabara M, et al. 1997. Comparison of the primary signs induced by experimental exposure to either a pneumotrophic or a "limping" strain of feline calicivirus. Veterinary Microbiology 56:33-45.

Prevalence

  • Bannasch MJ, Foley JE. 2005. Epidemiologic evaluation of multiple respiratory pathogens in cats in animal shelters. J Feline Med Surg 7:109-119
  • Binns SH, Dawson S, Speakman AJ, et al. 2000. A study of feline upper respiratory tract disease with reference to prevalence and risk factors for infection with feline calicivirus and feline herpesvirus. J Fel Med Surg 2:123-133
  • Coyne KP, Dawson S, Radford AD, et al. 2006. Long-term analysis of feline calicivirus prevalence and viral shedding patterns in naturally infected colonies of domestic cats. Veterinary Microbiology 118:12-25
  • Helps CR, Lait P, Damhuis A, et al. 2005. Factors associated with upper respiratory tract disease caused by feline herpesvirus, feline calicivirus, Chlamydophila felis and Bordetella bronchiseptica in cats: experience from 218 European catteries. Veterinary Record 156:669-673.

Chronic stomatitis

  • Healey KA, Dawson S, Burrows R, et al. 2007. Prevalence of feline chronic gingivo-stomatitis in first opinion veterinary practice. Journal of Feline Medicine and Surgery 9:373-381.

FCV-VSD first report

  • Pedersen NC, Elliott JB, Glasgow A, et al. 2000. An isolated epizootic of hemorrhagic-like fever in cats caused by a novel and highly virulent strain of feline calicivirus. Veterinary Microbiology 73:281-300.

Author

Find out more about Professor Alan Radford.